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1.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 253-261, 2024.
Artigo em Chinês | WPRIM | ID: wpr-1006578

RESUMO

Cerebral ischemia/reperfusion injury (CIRI) is a complex cascade reaction process in which the blood flow and oxygen supply of brain tissue in the infarcted area recover after cerebral ischemia, resulting in secondary injury of ischemic brain tissue. At present, thrombolysis as soon as possible and restoration of cerebral blood supply are still the only strategies for the treatment of stroke, but a considerable number of patients' symptoms will be more serious after reperfusion, making patients face adverse outcomes such as neurological function injury and even death and seriously affecting the quality of life and safety of patients. Therefore, an in-depth exploration of the mechanism and treatment strategy of CIRI has important clinical significance. The phosphatidylinositol 3- kinase (PI3K)/protein kinase B (Akt) signaling pathway is one of the classic anti-apoptosis/reproductive-promoting signal transduction pathways, which is responsible for cell proliferation, growth, and differentiation. It is the key cascade signaling pathway of CIRI, located at the core site in many mechanisms such as mitochondrial disorder, apoptosis, autophagy, oxidative stress, and inflammation. It is closely related to the occurrence and development of CIRI. Traditional Chinese medicine has been used in the clinical treatment of stroke and its complications for thousands of years, and the clinical effect of traditional Chinese medicine in the prevention and treatment of CIRI has been affirmed by a large number of research results in recent years. It is further clarified that the monomers, active components, and their compound prescriptions of traditional Chinese medicine can directly or indirectly regulate the PI3K/Akt signaling pathway by virtue of the biological advantages of multi-targets, multi-components, and multi-pathways and play an overall protective role in CIRI. By analyzing the related research progress of traditional Chinese medicine in China and abroad in recent years, the authors summarized the role and mechanism of regulating the PI3K/Akt signaling pathway in the prevention and treatment of CIRI, so as to provide further theoretical basis for the study of the mechanism of clinical prevention and treatment of CIRI.

2.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 101-108, 2024.
Artigo em Chinês | WPRIM | ID: wpr-1006560

RESUMO

ObjectiveTo investigate the promotional effect of astragaloside on the repair and healing of chronic non-healing wounds and its mechanism. MethodA total of 60 male SD rats were constructed with full-layer skin defect wounds on the back, and except for the control (Con) group, the rest were constructed with non-healing wounds, which were then randomly divided into the sham-operation (sham) group, the low-dose astragaloside group, the high-dose astragaloside group, the astragaloside + LY294002 [phosphatidylinositol 3-kinase (PI3K) inhibitor] group, and the astragaloside + EX527 [silencing regulatory protein 1 (SIRT1) inhibitor] group. The percentage of wound area in each group was observed on the 2nd, 4th, 6th, and 8th days after wound molding. Collagen type Ⅰ alpha 1 (COL1A1) and alpha smooth muscle actin (α-SMA) expressions in the wound tissue were detected by immunofluorescence. Hematoxylin and eosin (HE) staining was performed to determine the pathological structure of the wound. The mRNA expression of inflammatory factors in the wound was measured by real-time polymerase chain reaction (Real-time PCR), and the expression of proteins related to the SIRT1/ nuclear factor (NF)-κB and PI3K/protein kinase B (Akt) signaling pathways in the wound was tested by Western blot. ResultCompared with the sham group, the percentage of postoperative wound area of rats in both low-dose and high-dose astragaloside groups gradually decreased with time, and the efficacy of the high-dose astragaloside group was better. Compared with the Con group, the fluorescence intensity of COL1A1 in wound tissue of the sham group decreased, while the expression of α-SMA increased. The epithelial tissue was severely damaged, with an increase in the thickness, and a large number of inflammatory cells were seen in the infiltration. The mRNA expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and inducible nitric oxide synthase (iNOS) was elevated. The protein expression of NF-κB p65, p-PI3K/PI3K, and p-Akt/Akt was elevated, while SIRT1 expression was decreased (P<0.05). Compared with the sham group, the fluorescence intensity of COL1A1 and α-SMA increased after astragaloside treatment. The number of epithelial cells increased, and the thickness decreased. The inflammatory cells decreased, and the amount of collagen increased. The mRNA expression of TNF-α, IL-1β, IL-6, and iNOS was decreased, and the protein expression of NF-κB p65, p-PI3K/PI3K, and p-Akt/Akt was decreased. SIRT1 was elevated, and the effect was better in the high-dose astragaloside group (P<0.05). Compared with the high-dose astragaloside group, inhibition of the PI3K/Akt and SIRT1 pathways by LY294002 and EX527 prevented the therapeutic efficacy of astragaloside on chronic non-healing wounds. ConclusionThe topical application of astragaloside significantly promotes the healing of chronic non-healing wounds in rats, and the mechanism may be related to the activation of the PI3K/Akt pathway and the SIRT1/NF-κB pathway.

3.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 99-109, 2024.
Artigo em Chinês | WPRIM | ID: wpr-1003413

RESUMO

ObjectiveTo investigate the effect of Tangzhi pills on the improvement of insulin resistance (IR) in the liver with type 2 diabetes (T2DM) by regulating phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway based on differential genes and its possible molecular mechanism. MethodT2DM rat models were prepared by high fat (HFD) diet combined with streptozotocin (STZ) intraperitoneal injection. The experiment was divided into blank group, model group, metformin hydrochloride group (0.18 g·kg-1), Tangzhi pills high (1.08 g·kg-1), medium (0.54 g·kg-1) and low (0.27 g·kg-1) dose groups. Rat serum, liver, and pancreatic tissue were collected, and the pathological tissue of the liver and pancreas was observed using hematoxylin-eosin (HE) staining. The fasting blood glucose level (FBG) was detected, and oral glucose tolerance (OGTT) tests were conducted. Enzyme-linked immunosorbent assay (ELISA) was used to detect fasting serum insulin (FINS) and glycated hemoglobin (GHb) levels in rats. IR homeostasis model index (HOMA-IR), β cellular homeostasis index (HOMA-β), and insulin sensitivity index (ISI) were calculated. Biochemical methods were used to determine the levels of triglyceride (TG), total cholesterol (TC), low-density lipoprotein (LDL-C), and high-density lipoprotein (HDL-C) in rat serum. Transcriptomics obtained differentially expressed mRNA from liver tissue and enriched differentially expressed pathways. Real-time reverse transcriptase polymerase chain reaction (Real-time PCR) was used to detect the mRNA expression of cyclic adenylate responsive element binding protein 3-like protein 2 antibody (CREB3l2), B-lymphocyte tumor 2 (Bcl-2), Toll-like receptor 2 (TLR2), cyclin-dependent kinase inhibitor 1A (CDNK1A), and DNA damage induced transcription factor 4-like protein (DDIT4) in liver tissue. Western blot was used to detect the protein expression of phosphorylated phosphatidylinositol 3-kinase (p-PI3K), phosphorylated protein kinase B (p-Akt), glucose transporter 4 (GLUT4), insulin receptor (INSR), and insulin receptor substrate 2 (IRS2). ResultThe pharmacodynamic experiment results showed that compared with model group, Tangzhi pills groups repaired liver and pancreatic tissue to varying degrees, reduced blood sugar (P<0.01), and promoted a decrease in serum FINS, GHb, and HOMA-IR (P<0.05, P<0.01). In addition, HOMA-β and ISI increased (P<0.05, P<0.01). The levels of TC, TG, and LDL-C decreased (P<0.05, P<0.01), while the levels of HDL-C increased (P<0.05, P<0.01). The transcriptomics experimental results confirmed that the PI3K/Akt signaling pathway was significantly expressed in both the blank group and model group, as well as in the high-dose Tangzhi pills group and model group. CDNK1A, DDIT4, CREB3l2, Bcl-2, and TLR2 were significantly differentially expressed mRNA during TG intervention in T2DM. Compared with the model group, the protein expression of p-PI3K, p-Akt, GLUT4, INSR, and IRS2 increased in all Tangzhi pills groups (P<0.01). The mRNA expression of CREB3l2, Bcl-2, and TLR2 increased (P<0.01), while that of CDNK1A and DDIT4 decreased (P<0.01). ConclusionTangzhi pills may regulate the PI3K/Akt signaling pathway based on the differential mRNA expression of CREB3l2, Bcl-2, TLR2, CDNK1A, and DDIT4, thereby improving IR in the liver with T2DM.

4.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 45-53, 2024.
Artigo em Chinês | WPRIM | ID: wpr-1016461

RESUMO

ObjectiveTo explore the molecular mechanism of Sanhuang Xiexintang (SHXXT) in protecting stress gastric ulcer (SGU) in rats through network pharmacology, molecular docking, and animal experiments. MethodThe active ingredients and corresponding targets in SHXXT were collected and screened from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP), Traditional Chinese Medicine Information Database (TCMID), Bioinformation Analysis Tool for Molecular Mechanism of Traditional Chinese Medicine (BATMAN-TCM), and Swiss Target Prediction database. SGU-related targets were screened from the Online Mendelian Inheritance in Man (OMIM), Therapeutic Target Database (TTD), GeneCards database, and PharmGKB database. Herbal-ingredient-target (H-C-T) network was constructed by using Cytoscape 3.9.1 software. Protein-protein interaction (PPI) of drug and disease intersection targets was analyzed by using the Protein Interaction Platform (STRING) database. Gene ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were conducted through the Database for Annotation Visualization and Integrated Discovery (DAVID). The active ingredients and key targets were validated using AutodockVina 1.2.2 molecular docking software, and the experimental results were further validated through animal experiments. ResultThe 55 active ingredients were screened, and 255 potential target genes for SHXXT treatment of SGU were predicted. The PPI analysis showed that protein kinase B (Akt), phosphatase and tensin homolog deleted on chromosome ten (PTEN), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and cyclooxygenase-2 (COX-2) are the core targets of SHXXT for protecting SGU. GO and KEGG analyses showed that SHXXT may affect the development of SGU by regulating various biological processes such as the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway and inflammatory processes. The molecular docking results showed that both the active ingredients and key targets had good binding ability. Animal experiments showed that compared with the blank group, the ulcer index (UI) of the model group was significantly increased (P<0.01), and the serum levels of TNF-α and IL-1β significantly increased (P<0.01). The phosphorylation level of PTEN in gastric mucosal tissue was significantly down-regulated (P<0.05). The phosphorylation levels of PI3K, Akt, and nuclear factor kappa-B (NF-κB) were significantly up-regulated (P<0.05). Compared with the model group, the UI of the treatment group was significantly reduced (P<0.01), and the serum levels of TNF-α and IL-1β were significantly reduced (P<0.01). The phosphorylation level of PTEN in gastric mucosal tissue was significantly up-regulated (P<0.01), and the phosphorylation levels of PI3K, Akt, and NF-κB were significantly downregulated (P<0.01). ConclusionThe application of network pharmacology prediction, molecular docking simulation, and animal experimental validation confirms that SHXXT regulates the PI3K/Akt/NF-κB signaling pathway to regulate the inflammatory response of rats and thus protects the gastric mucosa of SGU rats.

5.
Chinese Pharmacological Bulletin ; (12): 90-98, 2024.
Artigo em Chinês | WPRIM | ID: wpr-1013596

RESUMO

Aim To investigate the effect of ellagic acid (EA) on cognitive function in APP/PS 1 double- transgenic mice, and to explore the regulatory mechanism of ellagic acid on the level of oxidative stress in the hippocampus of double-transgenic mice based on the phosphatidylinositol 3-kinase/protein kinase B/glycogen synthase kinase-3 (PI3K/AKT/GSK-3 β) signaling pathway. Methods Thirty-two SPF-grade 6-month-old APP/PS 1 double transgenic mice were randomly divided into four groups, namely, APP/PS 1 group, APP/PS1 + EA group, APP/PS1 + LY294002 group, APP/PS 1 + EA + LY294002 group, with eight mice in each group, and eight SPF-grade C57BL/6J wild type mice ( Wild type) were selected as the blank control group. The APP/PS 1 + EA group was given 50 mg · kg

6.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 48-55, 2024.
Artigo em Chinês | WPRIM | ID: wpr-1013339

RESUMO

ObjectiveExploring the role of microRNA126 (miRNA126) in chronic kidney disease combined with atherosclerosis (CKD AS) by regulating the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway and the mechanism of Shenshuai Xiezhuo decoction in the intervention of CKD AS rats with 5/6 nephrectomy combined with high-fat feeding. MethodA total of 60 SD rats were randomly divided into sham operation group, model group, losartan group, and low, medium, and high dose groups of Shenshuai Xiezhuo decoction. The CKD AS rat model was established by 5/6 nephrectomy combined with high-fat feeding for 10 weeks. The low, medium, and high dose groups (6.0, 12.0, 24.0 g·kg-1·d-1) of Shenshuai Xiezhuo decoction and the losartan group (20 mg·kg-1·d-1) were gavaged, and the corresponding intervention was carried out for eight weeks. Then, the rats were killed, and samples were collected for corresponding detection. Fully automated biochemical analyzers were used to detect kidney function and blood lipids in rats: blood creatinine (SCr), blood urea nitrogen (BUN), total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) levels. Hematoxylin-eosin (HE) and Masson staining of aortic tissue and pathological observation under a light microscope were carried out, and autophagosomes and autophagy lysosomes were observed by transmission electron microscopy. Real-time fluorescence quantitative polymerase chain reaction (Real-time PCR) was used to determine the mRNA levels of miRNA126, PI3K, Akt, and mTOR in rats, and Western blot was used to determine the protein expression levels of phosphorylated (p)-PI3K, PI3K, p-Akt, Akt, p -mTOR, mTOR, benzyl chloride 1 (Beclin-1), and microtubule-associated protein light chain 3Ⅱ/Ⅰ (LC3Ⅱ/LC3Ⅰ). ResultCompared with the sham operation group, the serum SCr, BUN, TC, TG, and LDL-C in the model group were significantly increased (P<0.01). Compared with the model group, the SCr, BUN, TC, TG, and LDL-C were decreased in the losartan group and low, medium, and high dose groups of Shenshuai Xiezhuo decoction (P<0.05). Compared with the sham operation group, thickening plaques, infiltration of mononuclear macrophages, a small number of foam cells, disordered arrangement of smooth muscle fibers in the tunica media, and increased collagen fibers were observed in the model group, and the lesions in the losartan group and Shenshuai Xiezhuo decoction groups were alleviated compared with those in the model group. Compared with the model group, the number of autophagosomes and autophagy lysosomes increased in the medium and high dose groups of Shenshuai Xiezhuo decoction. Compared with the sham operation group, the expression of miRNA126 in the aortic tissue of the model group was significantly decreased (P<0.01), and the mRNA expressions of PI3K, Akt, and mTOR were significantly increased (P<0.01). Compared with the model group, the expression of miRNA126 in the aortic tissue of rats in high, medium, and low dose groups of Shenshuai Xiezhuo decoction and losartan group was significantly increased (P<0.01), while the mRNA expressions of PI3K, Akt, and mTOR were significantly decreased (P<0.01). Compared with the sham operation group, the protein expressions of p-PI3K, PI3K, p-Akt, Akt, p-mTOR, and mTOR in the model group were significantly increased (P<0.01), while the protein levels of Beclin-1, LC3Ⅰ, and LC3Ⅱ were significantly decreased (P<0.01). Compared with the model group, the protein expressions of p-PI3K, PI3K, p-Akt, Akt, p-mTOR, and mTOR in the losartan group and low, medium, and high dose groups of Shenshuai Xiezhuo decoction were decreased (P<0.05), while the protein levels of Beclin-1 and LC3Ⅱ/LC3Ⅰ were increased (P<0.05). ConclusionThe expression of miRNA126 is decreased in the aortic tissue of CKD AS rats, and the PI3K/Akt/mTOR pathway is activated to inhibit autophagy flux. Shenshuai Xiezhuo decoction regulates the PI3K/Akt/mTOR signaling pathway through miRNA126, restores the autophagy of aortic endothelial cells, protects the damage of CKD vessels, reduces the formation of As plaques, and slows the development of cardiovascular complications.

7.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 280-289, 2024.
Artigo em Chinês | WPRIM | ID: wpr-1012718

RESUMO

As one of the most difficult-to-cure neuropsychiatric disorders in clinical practice, schizophrenia is mainly manifested by behavioral abnormalities and multidimensional cognitive dysfunction, and the recurrence rate and disability rate of the disease are increasing year by year, which seriously affects patients' social functioning and quality of life, and even threatens the physical and mental health of the surrounding population. At present, the treatment of schizophrenia is mainly based on antipsychotic drugs combined with psychotherapeutic techniques, which have limited long-term therapeutic effects and a high relapse rate. Traditional Chinese medicine (TCM) boasts the advantages of multi-targets, multi-pathways, multi-links, and multi-levels, and plays a crucial role in the prevention and treatment of schizophrenia and its prognosis. Phosphatidylinositol 3-kinase (PI3K) is widely present in cells and is involved in the regulation of protein synthesis and apoptosis, and the different isoforms of protein kinase B (Akt) are of great significance in cell growth, oxidative stress, neuronal development and other processes. In recent years, a large number of studies have found that the PI3K/Akt signaling pathway is closely related to schizophrenia. Through regulating the PI3K/Akt signaling pathway, TCM monomers and TCM compounds mainly affect key signaling molecules such as mammalian target of rapamycin (mTOR), glycogen synthase kinase (GSK), glucose transporter (GLUT) for glucose uptake and transport, and nuclear factor E2-associated factor 2 (Nrf2), which organize the intracellular network of centers and regulate the formation and plasticity of neuronal synapse, and they play an important role in mitigating schizophrenia by regulating the processes of cell proliferation, migration and apoptosis of neurons, and has the advantages of multi-targets, all-encompassing and low toxicity. This article analyzes and explains the mechanism of TCM intervention in the PI3K/Akt signaling pathway against schizophrenia, in order to provide a theoretical basis and reference for the prevention and treatment of schizophrenia by TCM.

8.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 281-289, 2024.
Artigo em Chinês | WPRIM | ID: wpr-1011469

RESUMO

Cognitive impairment refers to the abnormality of the hippocampus, cortex and other parts of the brain, which is manifested by the decline of cognitive abilities such as learning, memory and attention. With the increase in people's work pressure and bad living habits, the incidence of cognitive impairment is getting higher and higher, which seriously affects people's normal life. However, there are adverse reactions such as gastrointestinal reactions and extrapyramidal reactions in Western drug treatment for cognitive impairment. Therefore, the development of a drug with relatively minimal adverse reactions is of great significance. Traditional Chinese medicine (TCM) has the characteristics of "multi-component, multi-pathway and multi-target", and the incidence of adverse reactions is relatively low. Studies have shown that the pathogenesis of cognitive impairment is closely related to oxidative stress, inflammation, apoptosis, autophagy and other processes of neurons in the cerebral cortex and hippocampus. Phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt) signal pathway plays an important role in the transmission of intracellular and intracellular signals, and in the regulation of cellular inflammation, apoptosis, autophagy, etc. TCM monomers, TCM extracts, and TCM compounds exert anti-inflammatory, antioxidant, anti-apoptotic and autophagy regulation effects by regulating the PI3K/Akt signaling pathway to improve cognitive impairment. This review first summarized the composition and regulatory process of the PI3K/Akt signaling pathway, and then discussed the research progress on the improvement of cognitive impairment through the improvement of oxidative stress, inflammation, apoptosis and autophagy of neurons. Finally, the recent research status of the regulation of this signaling pathway by TCM extracts, TCM monomers and TCM compounds to improve cognitive impairment was summarized. This study provides a theoretical basis for the future study of new TCM related to cognitive impairment.

9.
International Eye Science ; (12): 537-545, 2023.
Artigo em Chinês | WPRIM | ID: wpr-965773

RESUMO

AIM:To investigate the mechanism of curcumin inhibiting the choroidal neovascularization(CNV)of brown Norway(BN)rats.METHODS: CNV model of 36 BN rats was established through laser photocoagulation induction, and they were divided into 6 groups with 6 rats in each group. Normal group was fed normally with no intervention, while 532nm laser photocoagulation was used to establish a experimental CNV model in BN rats. Rats after modeling were respectively intervened for 14d and divided into model group, ranibizumab group, curcumin low [100mg/(kg·d)], medium [200mg/(kg·d)], and high [400mg/(kg·d)] dose group. The model group was given intragastric administration of saline for 14d, ranibizumab(10mg/mL, 0.2mL/dose)was injected at 2d after photocoagulation with 5μL once for rats in ranibizumab group, and different concentrations of curcumin were intragastrically administrated to the rats in low, medium and high groups for 14d. Fundus photography, fundus fluorescein angiography(FFA)and indocyanine green angiography(ICGA)examination were performed at 14d after photocoagulation. Ocular histopathological specimens of rats with CNV were made, and the central thickness of CNV were observed by HE staining. Ocular histopathological specimens were made, and the expressions of AKT/p-AKT/HIF-1α/VEGF signaling pathway-related proteins were observed by immunohistochemistry. The mRNA relative expressions of AKT/HIF-1α/VEGF factor in CNV tissues were detected by RT-qPCR, and the protein expressions of AKT/p-AKT/HIF-1α/VEGF factor in CNV tissues were detected by Western-blot.RESULTS: CNV generation rates in the model group, the ranibizumab group, and the low, medium and high-dose curcumin groups were 78.18%, 73.21%, 77.19%, 75.86%, 74.55%, respectively, which were higher than 70%. The average absorbance were 182.12±6.59, 119.22±8.03, 166.45±8.33, 164.34±5.69, 149.22±6.45, respectively; the ranibizumab group was significantly lower than the model group(P&#x0026;#x003C;0.05); the low-dose, medium-dose and high-dose groups were significantly higher than the ranibizumab group(P&#x0026;#x003C;0.05), and the curcumin high-dose group was significantly lower than the model group(P&#x0026;#x003C;0.05). HE staining showed that the retinal tissue structure of BN rats in normal group was clear and neatly arranged. The central thickness of CNV in the ranibizumab group was significantly reduced at 14d after photocoagulation compared with the model group(P&#x0026;#x003C;0.05); While the curcumin high-dose group was significantly reduced compared with the model group(P&#x0026;#x003C;0.05), but increased when compared with ranibizumab group(P&#x0026;#x003C;0.05). Immunohistochemistry results showed that AKT, p-AKT, HIF-1α, and VEGF factors were negatively expressed in the retinal tissue structure of BN rats in the normal group, and no brown-yellow reactants were found. The expression of AKT, p-AKT, HIF-1α, and VEGF factors in the model group were higher than that in the normal group at 14d after photocoagulation(P&#x0026;#x003C;0.05); the ranibizumab group was lower than the model group(P&#x0026;#x003C;0.05). While the expression of the curcumin high-dose group was significantly decreased compared with the model group(P&#x0026;#x003C;0.05), but significantly increased when compared with ranibizumab group(P&#x0026;#x003C;0.05). The mRNA results showed that the relative expression levels of AKT, HIF-1α and VEGF mRNA in the model group at 14d after photocoagulation were higher than those of the normal group(P&#x0026;#x003C;0.05); the ranibizumab group was lower than the model group(P&#x0026;#x003C;0.05). While curcumin high-dose group was significantly decreased compared with the model group(P&#x0026;#x003C;0.05), but significantly increased when compared with ranibizumab group(P&#x0026;#x003C;0.05). Western-blot results showed that there was no significant difference in the relative expression of AKT protein among each experimental groups at 14d after photocoagulation. The relative expression of p-AKT protein in the model group was significantly higher than that in the normal group(P&#x0026;#x003C;0.05); the ranibizumab group was significantly lower than the model group(P&#x0026;#x003C;0.05); the curcumin high-dose group was significantly lower than the model group(P&#x0026;#x003C;0.05). The relative expression levels of HIF-1α protein were significantly higher in the model group than in the normal group(P&#x0026;#x003C;0.05), and the ranibizumab group was lower than in the model group(P&#x0026;#x003C;0.05). The relative expression levels of HIF-1α protein was lower in the curcumin high-dose group than in the model group(P&#x0026;#x003C;0.05)but higher than ranibizumab group(P&#x0026;#x003C;0.05). The relative expression level of VEGF protein was significantly lower in the curcumin medium/high-dose group than in the model group(P&#x0026;#x003C;0.05).CONCLUSION: Curcumin at 400mg/(kg·d)has an inhibitory effect on CNV in BN rats. The mechanism may be closely related to inhibiting the activation of AKT/p-AKT/HIF-1α/VEGF signaling pathways.

10.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 186-194, 2023.
Artigo em Chinês | WPRIM | ID: wpr-964959

RESUMO

MethodIn the experiment, 46% vol Red Star Erguotou (10 mL·kg·d-1) was used to establish the AONFH rat model, and the intervention effect of JPHGP at different doses (2.5, 5.0, 10.0 g·kg-1) was observed. Jiangusheng pill (JGS, 1.53 g·kg-1) was selected as the positive control. After 8 weeks of administration, the bone histomorphometry of the femoral head was analyzed by Micro-CT imaging, and the area of medullary microvessels in the femoral head was detected by ink perfusion. The pathological change was observed by hematoxylin and eosin (HE) staining. The protein expressions of Platelet endothelial cell adhesion molecule-1 (CD31), VEGF, VEGFR2, PI3K, phosphor-Akt (p-Akt) and phosphatase and Tensin homologue deleted on chromosome 10 (PTEN) in the femoral head were determined by immunohistochemistry and Western blot. ResultCompared with normal group, the model group presented the fracture and thinning of trabeculae in the femoral head, increased empty bone lacunae, and elevated number and diameter of adipocytes (P<0.01). Micro-CT imaging revealed a decrease in bone mineral density (BMD), bone volume fraction (BV/TV), trabecular thickness (Tb.Th) and trabecular number (Tb.N) (P<0.05, P<0.01) while an increase in bone surface-to-volume ratio (BS/BV) and trabecular separation (Tb.Sp) (P<0.01). The results of ink perfusion showed that the area of medullary microvessels in the femoral head was reduced (P<0.01). Compared with model group, JPHGP lowered the empty bone lacunae rate as well as the number and diameter of adipocytes in the femoral head of AONFH rats. Micro-CT imaging indicated that JPHGP low-dose group had elevated BV/TV, Tb.Th and Tb.N (P<0.05, P<0.01) while decreased BS/BV (P<0.01), and there was an upward trend in BMD while a downward trend in Tb.Sp, but without statistical difference. In addition, JPHGP medium- and high-dose groups had a rise in BMD, BV/TV, Tb.Th and Tb.N (P<0.05, P<0.01), a decrease in BS/BV and Tb.Sp (P<0.05, P<0.01) and enlarged area of medullary microvessels in the femoral head (P<0.05, P<0.01). The expressions of CD31, VEGF, VEGFR2, PI3K, p-Akt in the model group were lower than those in the normal group (P<0.01), and after medium and high doses of JPHGP treatment, the expressions of CD31, PI3K and p-Akt in the femoral head of rats were up-regulated (P<0.01) while the protein expression of PTEN was down-regulated (P<0.01). Moreover, JPHGP up-regulated the expressions of VEGF and VEGFR2 (P<0.05, P<0.01). ConclusionJPHGP can repair the vascular injury in AONFH, and its mechanism may be related to the activation of VEGF/VEGFR2/PI3K/Akt signaling pathway. This study provides certain scientific basis and reference for the clinical application of JPHGP. ObjecctiveTo observe the repair effect of Jianpi Huogu prescription (JPHGP) on vascular injury in experimental alcohol-induced osteonecrosis of femoral head (AONFH), and to explore its mechanism based on vascular endothelial growth factor (VEGF)/VEGFR2/phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway.

11.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 10-18, 2023.
Artigo em Chinês | WPRIM | ID: wpr-964940

RESUMO

ObjectiveTo explore the mechanism of Dihuang Yinzi in improving astrocyte injury and glycolysis in Alzheimer's disease (AD) mice via regulating the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, thereby improving the cognitive function of AD mice. MethodForty male APP/PS1 transgenic mice aged four months were randomly divided into a model group and a model + Dihuang Yinzi (0.25 g·kg-1) group, with 20 mice in each group. Forty C57BL/6J mice with the same background and same age were randomly divided into a control group and a control + Dihuang Yinzi (0.25 g·kg-1) group, with 20 mice in each group. The mice in the control + Dihuang Yinzi group and the model + Dihuang Yinzi group were administered with Dihuang Yinzi by gavage, and those in the control group and the model group received an equal volume of sterilized normal saline, once a day for 150 days. Morris water maze test was performed to test the ability of navigation and space exploration of mice. The protein expression of p-PI3K, PI3K, p-Akt, Akt, phosphofructokinase-1 (PFK-1), and aldehyde dehydrogenase 3 family member B2 (ALDH3B2) in mouse brain tissues was measured by Western blot. An immunofluorescence assay was performed to detect astrocyte morphology and the expression level of ALDH3B2. ResultAs compared with the control group, the model group showed prolonged escape latency during the 2nd to 5th days of the location-based navigation (P<0.05, P<0.01), reduced number of times crossing the target area of the platform, shortened residence time in the target quadrant (P<0.05, P<0.01), prolonged residence time in the opposite quadrant (P<0.05), increased surface area of the cell body and total length of cell protrusions of astrocytes (P<0.05, P<0.01), and down-regulated protein expression of p-PI3K, p-Akt, ALDH3B2, and PFK-1 (P<0.01), while the above experimental indexes were not significantly different in the control + Dihuang Yinzi group. Compared with the model group, the model + Dihuang Yinzi group showed shortened escape latency of APP/PS1 mice during the 2nd to 5th days of the location-based navigation (P<0.05, P<0.01), increased number of times crossing the platform, prolonged target quadrant residence time (P<0.05, P<0.01), shortened residence time in the opposite quadrant (P<0.05), reduced surface area of the cell body and total length of cell protrusions of astrocytes (P<0.05), and up-regulated protein expression of p-PI3K, p-Akt, ALDH3B2, and PFK-1 (P<0.01). ConclusionDihuang Yinzi can improve the learning and memory ability of AD mice by activating the PI3K/Akt signaling pathway and up-regulating the protein expression of PFK-1 and ALDH3B2 to protect against astrocyte injury in brain tissues and improve glycolysis.

12.
Chinese Acupuncture & Moxibustion ; (12): 679-683, 2023.
Artigo em Chinês | WPRIM | ID: wpr-980778

RESUMO

OBJECTIVE@#To observe the effect of electroacupuncture (EA) on liver protein kinase B (Akt)/forkhead box transcription factor 1 (FoxO1) signaling pathway in Zucker diabetic fatty (ZDF) rats, and to explore the possible mechanism of EA on improving liver insulin resistance of type 2 diabetes mellitus.@*METHODS@#Twelve male 2-month-old ZDF rats were fed with high-fat diet for 4 weeks to establish diabetes model. After modeling, the rats were randomly divided into a model group and an EA group, with 6 rats in each group. In addition, six male Zucker lean (ZL) rats were used as the blank group. The rats in the EA group were treated with EA at bilateral "Zusanli" (ST 36), "Sanyinjiao" (SP 6), "Weiwanxiashu" (EX-B 3), and "Pishu" (BL 20). The ipsilateral "Zusanli" (ST 36) and "Weiwanxiashu" (EX-B 3) were connected to EA device, continuous wave, frequency of 15 Hz, 20 min each time, once a day, six times a week, for a total of 4 weeks. The fasting blood glucose (FBG) in each group was compared before modeling, before intervention and after intervention; the serum levels of insulin (INS) and C-peptide were measured by radioimmunoassay method, and the insulin resistance index (HOMA-IR) was calculated; HE staining method was used to observe the liver tissue morphology; Western blot method was used to detect the protein expression of Akt, FoxO1 and phosphoenolpyruvate carboxykinase (PEPCK) in the liver.@*RESULTS@#Before intervention, compared with the blank group, FBG was increased in the model group and the EA group (P<0.01); after intervention, compared with the model group, FBG in the EA group was decreased (P<0.01). Compared with the blank group, the serum levels of INS and C-peptide, HOMA-IR, and the protein expression of hepatic FoxO1 and PEPCK were increased (P<0.01), while the protein expression of hepatic Akt was decreased (P<0.01) in the model group. Compared with the model group, the serum levels of INS and C-peptide, HOMA-IR, and the protein expression of hepatic FoxO1 and PEPCK were decreased (P<0.01), while the protein expression of hepatic Akt was increased (P<0.01) in the EA group. In the model group, the hepatocytes were structurally disordered and randomly arranged, with a large number of lipid vacuoles in the cytoplasm. In the EA group, the morphology of hepatocytes tended to be normal and lipid vacuoles were decreased.@*CONCLUSION@#EA could reduce FBG and HOMA-IR in ZDF rats, improve liver insulin resistance, which may be related to regulating Akt/FoxO1 signaling pathway.


Assuntos
Masculino , Animais , Ratos , Ratos Zucker , Proteínas Proto-Oncogênicas c-akt/genética , Diabetes Mellitus Tipo 2/terapia , Resistência à Insulina , Peptídeo C , Eletroacupuntura , Fígado , Transdução de Sinais , Insulina , Lipídeos
13.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 42-51, 2023.
Artigo em Chinês | WPRIM | ID: wpr-984582

RESUMO

ObjectiveTo explore the mechanisms of internal treatment (Renshen Baidusan), external treatment (Yurui Enema), and combination of the two methods in treating intestinal mucosal injury in the rat model of ulcerative colitis (UC) from the changes of phosphatidylinositol-3 kinase (PI3K)/protein kinase B (Akt)/nuclear factor-κB (NF-κB) pathway. MethodFifty SPF-grade SD rats were randomized into blank, model, Renshen Baidusan (15.6 g·kg-1), Yurui Enema (25 g·kg-1), and combined treatment (15.6 g·kg-1 Renshen Baidusan + 25 g·kg-1 Yurui Enema) groups (n=10). The rat model of UC was established in other groups except the blank group by 2,4, 6-trinitrosulfonic acid (TNBS)/ethanol. The rats were administered with corresponding drugs once a day for 14 consecutive days since the 8th day after modeling. The histopathological changes of colon were observed by hematoxylin-eosin (HE) staining. Enzyme-linked immunosorbent assay (ELISA) was employed to measure the levels of tumor necrosis factor (TNF)-α, interferon (IFN)-γ, interleukin (IL)-4, and IL-10 in the colon tissue. The apoptosis of colon epithelial cells was detected by terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL). The location and expression of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), TNF-α, and IL-6 in the colon tissue were examined by immunohistochemistry. Real-time quantitative fluorescence polymerase chain reaction (Real-time PCR) and Western blot were employed to determine the mRNA and protein levels, respectively, of the proteins in the PI3K/Akt/NF-κB pathway in the colon tissue. ResultIn the model group, HE staining showed a large number of inflammatory cell infiltration in the mucosa and submucosa. Compared with the blank group, the model group showed elevated levels of TNF-α and IFN-γ and lowered levels of IL-4 and IL-10 in the colon tissue, increased apoptosis rate of colon epithelial cells, increased positive expression of Bax, TNF-α, and IL-6, and decreased positive expression of Bcl-2 (P<0.05). Moreover, the model group showed up-regulated mRNA levels of PI3K, Akt, and NF-κB and protein levels of PI3K, p-PI3K, Akt, p-Akt, p65, p-p65, Bax, and cleaved Caspase-3, increased Bax/Bcl-2 and cleaved Caspase-3/Caspase-3 ratios, and down-regulated protein levels of NF-κB suppressor protein α(IκBα), Bcl-2, and Caspase-3 in the colon tissue (P<0.05). Compared with the model group, the internal treatment, the external treatment, and the combination (referred to as the three groups) alleviated the colonic mucosal injury, lowered the levels of TNF-α and IFN-γ and elevated the levels of IL-4 and IL-10 in the colon tissue, decreased the apoptosis rate of colon cells, inhibited the positive expression of Bax, TNF-α, and IL-6, and promoted the positive expression of Bcl-2 (P<0.05). Furthermore, the combination group down-regulated the mRNA level of PI3K (P<0.05). The three groups down-regulated the mRNA levels of Akt and NF-κB and the protein levels of p-PI3K, Akt, p-Akt, p65, p-p65, Bax, and cleaved Caspase-3 in the colon tissue, decreased the Bax/Bcl-2 and cleaved Caspase-3/Caspase-3 ratios, and up-regulated the protein levels of IκBα, Bcl-2, and Caspase-3 (P<0.05). ConclusionRenshen Baidusan, Yurui Enema, and their combination may inhibit the activation of PI3K/Akt/NF-κB signaling pathway and regulate the expression of genes and proteins related to this pathway to achieve anti-inflammatory and anti-apoptotic effects, thus restoring the intestinal mucosal barrier function of UC rats.

14.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 253-263, 2023.
Artigo em Chinês | WPRIM | ID: wpr-997679

RESUMO

Osteoporosis (OP), a common systemic skeletal disease in the elderly, is characterised by bone loss and bone microstructural degeneration. Its clinical manifestations include increased bone fragility and bone pain. Furthermore, OP increases the risk of fracture due to the high bone fragility, which leads to lifelong disability or death, imposing a heavy economic and psychological burden on the patients and their families. The pathogenesis of OP is extremely complex and associated with a variety of factors such as proliferation and differentiation of osteoblasts, impairment of osteoclast activity and function, and abnormalities in autophagy activation. Recent studies have found that mammalian target of rapamycin (mTOR) signaing pathway is involved in the regulation of bone homeostasis, which can promote bone formation and improve bone metabolism and bone microstructure by regulating osteoblast proliferation and differentiation and osteoclast function and activating cellular autophagy, thus playing a crucial role in the prevention and treatment of OP. The prevention and treatment of OP with Chinese medicine has a long history, clear efficacy, multiple targets of action, low adverse effects, and wide medicine sources. Therefore, this paper briefly describes the role of mTOR signaling pathway in the development of OP by reviewing the latest research reports and summarizes in detail the latest research results on the treatment of OP with Chinese medicine extracts and prescriptions via the mTOR signaling pathway. This review aims to provide a basis for the in-depth research on the relationship between mTOR signaling pathway and OP and the clinical application of traditional Chinese medicine in the prevention and treatment of OP.

15.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 218-226, 2023.
Artigo em Chinês | WPRIM | ID: wpr-997675

RESUMO

Non-small cell lung cancer (NSCLC) is a malignant tumor of the respiratory system with a high incidence. The early symptoms are not typical, and most patients are diagnosed at an advanced stage, which seriously threatens the lives and health of people. Surgery, chemotherapy, and targeted therapy are the main means of treatment at present, but the consequent drug resistance and adverse reactions restrict these treatment methods with certain limitations. In recent years, with the development of traditional Chinese medicine (TCM) in tumor resistance, TCM has attracted extensive attention for its obvious therapeutic effect and fewer adverse reactions. Numerous signaling pathways are involved in the formation and development of NSCLC, where phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway is one of the key regulatory pathways. The PI3K/Akt/mTOR signaling pathway affects the proliferation, invasion, and metastasis of NSCLC cells by affecting the cycle, inhibiting the apoptosis, inhibiting the autophagy of tumor cells, and promoting tumor neovascularization. As revealed by the recent literature, Chinese medicine plays an indispensable role in NSCLC cell autophagy, cell cycle, apoptosis, invasion and metastasis, neovascularization, and reversal of drug resistance by regulating the PI3K/Akt/mTOR signaling pathway. Although some Chinese medicinal extracts or compounds have made great breakthroughs in some mechanisms of action in the treatment of NSCLC, these studies only remain at the level of in vitro cell experiments and animal studies in vivo. Researchers are faced with the great challenge of "transforming the research results of Chinese medicines into clinical applications". Based on the current research status in China and abroad, this paper reviewed Chinese medicine in the intervention in NSCLC through the regulation of PI3K/Akt/mTOR signaling pathway in recent years, in order to open up new ideas for NSCLC drug therapy research and also provide a useful reference for further mechanism research.

16.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 71-78, 2023.
Artigo em Chinês | WPRIM | ID: wpr-996812

RESUMO

ObjectiveTo study the effect and underlying mechanism of Stemona tuberosa alkaloids on the proliferation and apoptosis of human non-small cell lung cancer NCI-H460 cells. MethodNon-small cell lung cancer NCI-H460 cells were divided into a blank group and S. tuberosa alkaloids groups (50, 100, 150, 200, and 250 mg·L-1). The effect of S. tuberosa alkaloids on the proliferation of human NCI-H460 cells was observed by thiazolyl blue tetrazolium bromide (MTT) assay and colony formation assay. Cell apoptosis was observed by Hoechst 33258 staining and flow cytometry. Real-time fluorescence-based polymerase chain reaction (Real-time PCR) was used to detect the effect of S. tuberosa alkaloids on the mRNA expression of cysteinyl aspartate-specific protease 3 (Caspase-3), B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), and epidermal growth factor receptor (EGFR). The protein expression levels of Caspase-3, Bax, Bcl-2, protein kinase B (Akt), phosphorylated (p-)Akt, EGFR, c-Jun N-terminal kinase (JNK), p-JNK, p38 mitogen-activated protein kinase (p38 MAPK), and p-p38 MAPK were measured by Western blot. ResultCompared with the blank group, the S. tuberosa alkaloids groups showed increased inhibition rate on cell proliferation (P<0.01), reduced number of cell clones formed and the rate of cell clonal formation (P<0.05, P<0.01), and increased karyopyknosis, cytoplasmic aggregation, and cell apoptosis rate (P<0.01). The S. tuberosa alkaloids groups at 100, 150, 200, and 250 mg·L-1 showed increased Caspase-3 mRNA expression (P<0.05), decreased EGFR mRNA expression (P<0.05, P<0.01), up-regulated protein expression of Caspase-3 and p-JNK (P<0.01), and down-regulated protein expression of EGFR and p-Akt (P<0.05, P<0.01). Additionally, compared with the blank group, the S. tuberosa alkaloids groups showed increased expression of Bax mRNA (P<0.01), decreased expression of Bcl-2 mRNA (P<0.01), up-regulated protein expression of Bax and p-p38 MAPK (P<0.01), and down-regulated protein expression of Bcl-2 (P<0.01). ConclusionsS. tuberosa alkaloids can inhibit proliferation and induce apoptosis of human non-small cell lung cancer NCI-H460 cells, and the mechanism may be related to the inhibition of EGFR protein expression and phosphorylation of Akt protein, as well as the activation of the JNK/p38 MAPK signaling pathway.

17.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 109-115, 2023.
Artigo em Chinês | WPRIM | ID: wpr-979455

RESUMO

ObjectiveTo investigate the effects and molecular mechanism of ursolic acid on the proliferation and apoptosis of colorectal cancer cells. MethodThe proliferation inhibition rate of human colorectal cancer RKO cells treated with different concentrations of ursolic acid (0, 5, 10, 15, 20, 25, 30 μmol·L-1) was detected by cell counting kit-8 (CCK-8), and the half maximal inhibitory concentration (IC50) at 24 h and 48 h was calculated. According to the IC50 of RKO cells treated with ursolic acid for 24 h, two concentrations were selected for subsequent experiments. The colony formation assay was used to detect the proliferation ability of the cells and flow cytometry was used to detect the apoptosis rate and cell cycle arrest after treatment of RKO cells with ursolic acid. After treatment of RKO cells with ursolic acid for 24 hours, the expression of B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax) in RKO cells, Bcl-2 in Raji cells, PMA responsive gene in T lymphocyte (Noxa), cyclin-dependent kinase inhibitor 1A (p21), cyclin-dependent kinase inhibitor 1B (p27), cyclin-dependent kinase 4 (CDK4), protein kinase B (Akt), phosphorylated Akt (p-Akt), forkhead transcription factor O3a (FoxO3a), and phosphorylated FoxO3a (p-FoxO3a) was determined by Western blot. ResultCompared with the blank group, the ursolic acid groups could inhibit the viability of RKO cells (P<0.05, P<0.01), and the colony formation rates of RKO cells in the ursolic acid groups were reduced (P<0.05, P<0.01) in a concentration-dependent manner. The cells in the ursolic acid group (20 μmol·L-1) experienced cell cycle arrest, which increased in the early stage of synthesis, ie, the G0/G1 phase (P<0.05) as compared with the results in the blank group. Compared with the blank group, the ursolic acid groups (15 and 20 μmol·L-1) showed increased protein expression of p21 and p27, decreased expression of CDK4 protein (P<0.05, P<0.01), and increased apoptosis rate, and the ursolic acid group (20 μmol·L-1) showed increased protein expression of Bax and Noxa and decreased expression of Bcl-2 (P<0.05, P<0.01). In terms of mechanism, compared with the blank group, the ursolic acid group (20 μmol·L-1) down-regulated the expression of p-Akt protein and up-regulated the expression of p-FoxO3a (P<0.05, P<0.01), and there was no significant change in the total protein of Akt and FoxO3a. ConclusionUrsolic acid can effectively inhibit the proliferation of colorectal cancer RKO cells and promote cell apoptosis, which may be related to the Akt/FoxO pathway.

18.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 1-11, 2023.
Artigo em Chinês | WPRIM | ID: wpr-978445

RESUMO

ObjectiveTo explore the effect and mechanism of Zuojinwan (ZJW) in the treatment of ulcerative colitis (UC) through network pharmacology and experimental validation. MethodUsing network pharmacology and molecular docking, the active components and potential mechanism of ZJW in treating UC were preliminarily identified. Forty-eight male C57BL/6J mice were randomly divided into a normal group, a model group, a sulfasalazine group (300 mg·kg-1), and low-, medium-, and high-dose ZJW groups (1.82, 3.64, 7.28 g·kg-1). The UC model was induced by dextran sulfate sodium (DSS), and oral administration of drugs began on the third day of modeling, lasting for 7 days. The general condition of mice was observed daily, and the disease activity index (DAI) was evaluated. Hematoxylin-eosin (HE) staining was performed to observe histopathological changes in colon tissue. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 in mouse serum. The molecular mechanism was validated using Western blot. ResultNetwork pharmacology predicted that the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway might be a key pathway in the regulation of UC by ZJW. Molecular docking results showed good binding ability between the key components of ZJW and core targets. Animal experiment results showed that compared with the normal group, the model group had shortened colon length (P<0.01), increased DAI scores, spleen index, colon tissue pathology scores, and levels of TNF-α and IL-6 in serum (P<0.05, P<0.01), increased PI3K, phosphorylated Akt (p-Akt), and B-cell lymphoma-2 (Bcl-2)-associated X protein (Bax) expression in colon tissue (P<0.05, P<0.01), and decreased serum IL-10 levels and colon tissue Bcl-2 protein expression (P<0.01). Compared with the model group, the ZJW groups showed significant improvement in UC symptoms, relieved colon tissue pathological damage, downregulated levels of inflammatory cytokines TNF-α and IL-6 in serum (P<0.01), inhibited expression of PI3K, p-Akt, and Bax proteins in colon tissue (P<0.05, P<0.01), and increased serum IL-10 levels and colon tissue Bcl-2 protein expression (P<0.01), with the high-dose group showing the best effect. ConclusionZJW effectively alleviates DSS-induced UC, and its mechanism may be related to the inhibition of the PI3K/Akt signaling pathway and regulation of apoptosis-related protein expression.

19.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 254-263, 2023.
Artigo em Chinês | WPRIM | ID: wpr-973768

RESUMO

Colorectal cancer (CRC), as the third most common cancer in the world, develops from the colonic and rectal epithelial cells. With the rapid development of the global economy, the incidence of CRC in developing countries has been increasing year by year. In the past few years, although preventive colonoscopy screening has improved the survival rate of CRC patients, the majority of cases are still detected after symptoms appear. Currently, the clinical treatment of CRC carries high surgical risks and is prone to recurrence, while radiotherapy and chemotherapy have significant side effects and cause a heavy psychological burden on patients. Therefore, there is currently no ideal treatment protocol for CRC. The phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway, as a classical oncogenic pathway, provides potential for the diagnosis and treatment of various malignant diseases, and offers a new direction for the treatment of CRC. In recent years, traditional Chinese medicine (TCM) has become a major focus in cancer treatment due to its advantages in "preventing and treating diseases" and its multiple components, targets, and pathways. Its advantages in having fewer side effect complement western medicine in treatment. Multiple studies have shown that Chinese medicinal monomers and compound formulas can inhibit the proliferation, invasion, migration, and angiogenesis of CRC cells, promote apoptosis and autophagy of cancer cells, and slow down the development of CRC by intervening in the PI3K/Akt signaling pathway, thereby achieving the therapeutic effect on CRC. In recent years, the research progress related to this has been updating rapidly. Previous literature failed to timely incorporate the latest research results, which brought many inconveniences to the literature search of many scholars. Therefore, this article summarized the relevant information from PI3K/Akt pathway, the association between the PI3K/Akt pathway and CRC, and the progress of TCM intervention in the treatment of CRC to provide references for the development of CRC in molecular biology and the clinical development of new drugs in the future.

20.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 230-240, 2023.
Artigo em Chinês | WPRIM | ID: wpr-973766

RESUMO

Hepatic fibrosis is a pathological reparative response of the liver to chronic injury and a crucial step in the progression of chronic liver disease, characterized mainly by the activation of hepatic stellate cells and diffuse deposition of extracellular matrix. Currently, there is no ideal specific drug for the treatment of liver fibrosis in clinical practice. In recent years, with the development and progress of traditional Chinese medicine (TCM) in the treatment of liver fibrosis, TCM has been widely recognized for its significant therapeutic effect and fewer adverse reactions. The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway is an important pathway that affects the formation and development of liver fibrosis. It mainly plays a role in liver fibrosis by inhibiting the activation and proliferation of hepatic stellate cells, promoting their apoptosis, reducing oxidative stress in liver cells, decreasing the deposition of extracellular matrix, and enhancing liver cell autophagy. This article summarized the mechanisms by which Chinese medicinal monomers regulated the PI3K/Akt pathway to exert their effects on liver fibrosis and their synergistic effects with other signaling pathways, providing a theoretical basis and references for the development of new drugs for the treatment of liver fibrosis with TCM.

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