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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.
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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.
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ObjectiveKey microRNAs （miRNAs） of colorectal adenoma （CRA） were identified and analyzed by bioinformatics methods， and differentially expressed genes （DEGs） were screened to construct regulatory relationships. The mechanism of Xiezhuo Jiedu recipe in preventing CRA was speculated and verified by animal experiments. MethodThe miRNAs dataset GSE50194 was obtained from the Gene Expression Omnibus （GEO） database of intestinal mucosal tissue of CRA patients， and the differentially expressed miRNAs were screened by GEO2R and Excel. TargetScan， miRTarbase， and miRDB databases were used to predict the target genes of the differentially expressed miRNAs， and an intersection was obtained. Key DEGs were screened through the STRING database and Cytoscape software， and the TRRUST database was used to predict downstream binding transcription factors （TFs）. The mRNA intersection was enriched by gene ontology （GO） and Kyoto encyclopedia of genes and genomes （KEGG） in the Metascape database. DIANA TOOLS were applied to perform KEGG enrichment analysis of key miRNAs， and the key signaling pathways were selected for animal experiments. In animal experiments， the CRA mice model was established by using sodium glycan sulfate （DSS） drinking combined with intraperitoneal injection of azomethane oxide （AOM）， and Xiezhuo Jiedu recipe and aspirin were given by intragastric administration at the same time. The experiment lasted for nine weeks. The pathological changes in intestinal tissue were observed by hematoxylin-eosin （HE） staining. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of miR-34a-5p in adenoma tissue. Protein expression levels of phosphatidylinositol 3-kinase （PI3K）， protein kinase B （Akt）， phosphoryl-PI3K （p-PI3K）， phosphoryl-Akt （p-Akt）， and B cell lymphoma （Bcl）-2 were detected by Western blot. The expression of Cyclin D1 （CCND1） was detected by immunohistochemistry （IHC）. In situ terminal transferase labeling （TUNEL） was used to detect apoptosis of adenoma tissue cells. ResultThe GEO database screened the GSE50194 dataset， and miR-34a-5p was selected as the research object from CRA and normal tissue. A total of 93 DEGs were selected. Among them， GO and KEGG enrichment analyses were closely related to biological processes such as transcriptional regulatory complex， RNA polymerase Ⅱ transcriptional regulatory complex， enzyme-linked receptor protein signaling pathway， and DNA-binding transcriptional activator activity， cancer pathway， PI3K/Akt pathway， etc. miR-34a-5p is mainly enriched in PI3K/Akt， cell cycle， and colorectal cancer pathways. Five key DEGs were screened out through the Matescape database， among which Bcl-2 and CCND1 were the key DEGs of miR-34a-5p. Further screening of the TFs of key DEGs revealed that E2F transcription factor 1 （E2F1） and tumor protein P53 （TP53） were the main TFs of Bcl-2 and CCND1. Animal experiments showed that Xiezhuo Jiedu recipe could effectively up-regulate mRNA level of miR-34a-5p， down-regulate the expression of PI3K， Akt， Bcl-2， p-PI3K， and p-Akt proteins in the intestinal tissue of CRA mice， down-regulate the positive expression rate of CCND1， and increase the apoptosis rate of intestinal epithelial cells. ConclusionIt is speculated that Xiezhuo Jiedu recipe may inhibit the abnormal proliferation and promote the apoptosis of intestinal epithelial cells in CRA mice by regulating the miR-34a-5p/PI3K/Akt signaling pathway， thus playing a role in the prevention of CRA.
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ObjectiveTo observe the protective effect of Didang Xianxiong decoction on the kidneys of diabetic rats， its regulation on the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway， and its influence on podocyte apoptosis and explore the mechanism of Didang Xianxiong decoction in improving diabetic nephropathy. MethodThe diabetic model was established by a single intraperitoneal injection of streptozotocin （STZ） solution of 55 mg·kg-1. The successfully replicated model rats were randomly divided into the model group， Didang Xianxiong decoction group （8.10 g·kg-1）， Xiao Xianxiongtang group （4.05 g·kg-1）， Didangtang group （4.05 g·kg-1）， and alagebrium （ALT-711） group （3 mg·kg-1）， with six rats in each group. In addition， six rats were included in the blank group. After continuous administration for eight weeks， hematoxylin-eosin （HE） staining was used to observe the pathological changes in rats' kidney tissue. Masson staining was used to observe the degree of collagen deposition. Periodic acid-Schiff （PAS） staining was used to observe basement membrane lesions， and immunohistochemistry was used to detect the expression of phosphorylation （p）-PI3K and p-Akt proteins in rats' kidney tissue. The terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） method was used to detect podocyte apoptosis. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of PI3K and Akt in rats' kidney tissue. Western blot was used to detect the protein expression of PI3K， p-PI3K， Akt， p-Akt， B-cell lymphoma 2 （Bcl-2）， Bcl-2-associated X protein （Bax）， phosphorylation glycogen synthase kinase-3β （p-GSK-3β）， and Caspase-3 in the kidney tissue. ResultCompared with the normal group， the model group had compensatory expansion of glomeruli， proliferation of mesangial cells， a large amount of collagen deposition in the mesangial stroma， thickening of the basement membrane， decreased mRNA expression of PI3K and Akt， and inhibition of PI3K and Akt protein phosphorylation （P<0.01）. It also underwent enhanced apoptotic signaling， decreased expression of anti-apoptotic protein Bcl-2 （P<0.01）， and increased expression of Bax， p-GSK-3β， and Caspase-3 （P<0.01）. Compared with the model group， Didang Xianxiong decoction significantly improved kidney tissue pathology， increased mRNA expression of PI3K and Akt （P<0.01）， significantly up-regulated phosphorylation levels of PI3K and Akt proteins （P<0.01） and Bcl-2 expression （P<0.01）， downregulated the expression of Bax， p-GSK-3β， and Caspase-3 （P<0.01）， and weakened podocyte apoptotic signaling. ConclusionDidang Xianxiong decoction may promote the activation of the PI3K/Akt signaling pathway， inhibit podocyte apoptosis， and thus slow down the progression of diabetic nephropathy.
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BACKGROUND:In recent years,it has been found that some traditional Chinese medicine monomers can alleviate oxidative stress and apoptosis of the skin flap,promote vascular regeneration of the skin flap and prevent skin flap necrosis by activating autophagy. OBJECTIVE:To review the research progress of traditional Chinese medicine monomer regulating autophagy in preventing flap necrosis. METHODS:The Chinese and English key words were"traditional Chinese medicine(TCM),autophagy,skin flaps".The first author searched the relevant articles published in CNKI and PubMed databases from January 2010 to October 2022.A total of 196 articles were retrieved in the preliminary screening and then screened according to the inclusion and exclusion criteria.The quality assessment was conducted by reading the literature titles and abstracts.Finally,55 articles were summarized. RESULTS AND CONCLUSION:(1)The regulation of autophagy is mediated by AMPK/mTOR,PI3K/AKT and other signaling pathways.Activation of autophagy can alleviate the oxidative stress and apoptosis of the flap,promote the regeneration of blood vessels in the flap,and prevent flap necrosis.(2)Terpenoids(Betulinic acid,Andrographolide,Notoginseng Triterpenes,Catalpa),phenolic compounds(Resveratrol,Curcumin,Gastrodin),phenolic acids(Salvianolic acid B)and steroid compounds(Pseudoginsenoside F11)in traditional Chinese medicine monomers can alleviate oxidative stress and apoptosis of skin flap by regulating related signaling pathways to activate autophagy,promote skin flap angiogenesis and promote skin flap survival.(3)Studying the research progress of traditional Chinese medicine monomer to prevent flap necrosis by regulating autophagy can provide a reference and theoretical basis for traditional Chinese medicine to prevent flap necrosis and promote flap healing in the clinic.
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ObjectiveTo investigate the molecular mechanism of action of artemisinin in attenuating asthmatic airway inflammation and airway remodeling through the phosphoinositide 3-kinase（PI3K）/protein kinase B（Akt） signaling pathway. MethodFifty male SD rats were randomly divided into blank group， model group， and low-dose， medium-dose， and high-dose groups of artemisinin， with 10 rats in each group. The ovalbumin （OVA）-induced asthma model of the rats was established， and after successful modeling， the blank group and model group received tail vein injection of 1.0 mL·kg-1 normal saline， while the low-dose， medium-dose， and high-dose groups of artemisinin received tail vein injection of 12.5， 25， and 50 mg·kg-1 artemisinin daily for seven days. Airway resistance was measured by the acetylcholine chloride method. Cell number and species changes in the alveolar lavage fluid of each group were determined by flow cytometry. Morphological changes in airway endothelial tissue were determined by the hematoxylin-eosin （HE） staining method. Apoptosis was determined by CytoTox 96 method， and enzyme-linked immunosorbent assay （ELISA） method was used to determine the NOD-like receptor thermal protein domain associated protein 3 （NLRP3） inflammasome， interleukin-1β （IL-1β）， and interleukin-10 （IL-10） expression. Western blot method was used to detect the （p）-PI3K/p-Akt level in the alveolar bronchial tissue of each group. ResultCompared with the blank group， the total number of cells， total number of macrophages， total number of eosinophils， total number of lymphocytes， and total number of neutrophils were significantly higher in the model group （P<0.05）. HE staining showed that the airway mucosa of the rats had obvious edema， and a large number of inflammatory cells were infiltrated （P<0.05）. The rate of apoptosis was significantly higher （P<0.05）， and the levels of the inflammasome NLRP3， IL-1β， and IL-10 increased significantly （P<0.05）. p-PI3K/p-Akt level increased significantly （P<0.05）. Compared with the model group， the total number of cells， total number of macrophages， total number of eosinophils， total number of lymphocytes， and total number of neutrophils were significantly decreased after the intervention of artemisinin at low， medium， and high concentrations （P<0.05）. HE staining showed that the degree of edema of the airway mucosa of the rats was reduced， and the area of the inflammatory cell infiltration was drastically reduced （P<0.05）. The apoptosis rate was significantly reduced （P<0.05）， and the levels of the inflammasome NLRP3， IL-1β， and IL-10 decreased significantly （P<0.05）. p-PI3K/p-Akt level decreased significantly （P<0.05）. ConclusionArtemisinin significantly inhibits NLRP3 inflammasome activation， reduces cellular pyroptosis and inflammatory cell expression， and attenuates airway inflammatory manifestations and airway remodeling in asthmatic rats， which may be related to the regulation of p-PI3K/p-Akt， and the results may provide laboratory insights and basis for the treatment of bronchial asthma with artemisinin.
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Prostate cancer （PCa） is one of the most common malignant tumors in the male genitourinary system. The phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway is a carcinogenic pathway responsible for the migration， proliferation， and drug resistance of various cancers. In recent years， as the research on the pathogenesis of PCa is deepening， the role of the PI3K/Akt signaling pathway in the development of PCa has attracted much attention. Traditional Chinese medicine， comprehensively regulating multiple components， targets， and pathways， has shown great potential in the treatment of PCa. This article reviews the research progress of traditional Chinese medicine targeting the PI3K/Akt signaling pathway in the treatment of PCa and discusses the expression of the PI3K/Akt signaling pathway in PCa， which involves inhibiting apoptosis of PCa cells， promoting the cell cycle， invasion， and migration of PCa cells， promoting tumor tissue angiogenesis， and mediating the androgen receptor. Additionally， it summarizes the single Chinese medicines that target and regulate this pathway， including Hedyotis diffusa， Taxus chinensis， Bovisc Alculus， and Atractylodis Macrocephalae Rhizoma. The active ingredients of these Chinese medicines mainly include flavonoids， alkaloids， terpenes， polyphenols， lignans， and other compounds. The Chinese medicine compound prescriptions targeting the PI3K/Akt pathway mainly include Wenshen Sanjie prescription， Jianspi Lishi Huayu prescription， Yishen Tonglongtang， Qilan prescription， Xihuangwan， and modified Shenqi Dihuangtang. This review is expected to provide a scientific basis for deeply understanding the pathogenesis of PCa and identifying potential therapeutic targets， as well as to provide new ideas for clinical research and drug development for PCa.
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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.
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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.
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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.
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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
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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.
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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.
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ObjectiveTo explore the intervention effect and molecular mechanism of Dabufei decoction in Dunhuang formula combined with cisplatin on Lewis lung adenocarcinoma-bearing mice. MethodFifty C57BL/6J mice were used， with 10 randomly assigned to the blank group （without modeling）， and 40 subcutaneously inoculated with Lewis cells to establish a Lewis lung adenocarcinoma-bearing mouse model. These 40 mice were randomly divided into the following four groups （with 10 mice in each group）： Model group （equal volume of physiological saline）， cisplatin group （5 mg·kg-1）， Dabufei decoction group （14.35 g·kg-1·d-1）， and Dabufei decoction combined with cisplatin group （Dabufei decoction 14.35 g·kg-1·d-1 + cisplatin 5 mg·kg-1）. Each group was treated continuously for 14 days. The general condition of the mice was observed， body weight changes were recorded， and the tumor inhibition rate， spleen index， and thymus index were calculated. Peripheral blood white blood cell （WBC）， platelet （PLT）， and hemoglobin （HGB） were detected by routine blood tests. Flow cytometry was used to detect the expression of CD4+CD25+FoxP3+ regulatory T cells （Treg） and natural killer （NK） cells in the spleen. Western blot and real-time quantitative polymerase chain reaction （Real-time PCR） were used to determine the expression of proteins and mRNA related to the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR） signaling pathway in tumor tissues. ResultCompared with the blank group， the model group showed decreased body weight （P<0.05）， spleen index， and thymus index （P<0.05）， decreased percentage of NK cells in the spleen （P<0.05）， increased percentage of Treg cells （P<0.05）， and decreased counts of WBC， PLT， and HGB （P<0.05）. Compared with the model group， the Dabufei decoction group exhibited significant tumor growth inhibition， increased body weight， and reduced tumor weight （P<0.05）， increased percentage of NK cells （P<0.05）， decreased proportion of Treg cells （P<0.05）， and increased counts of WBC， PLT， and HGB （P<0.05）. In the cisplatin group， tumor growth was significantly inhibited， body weight significantly decreased （P<0.05）， and tumor weight significantly reduced （P<0.05）. The spleen index and thymus index decreased （P<0.05）， and the percentage of Treg cells significantly decreased （P<0.05）. The counts of WBC， PLT， and HGB significantly decreased （P<0.05）. In the Dabufei decoction combined with cisplatin group， tumor growth was significantly inhibited， and tumor weight significantly reduced （P<0.05）. The levels of phosphorylated PI3K， Akt， and mTOR proteins and mRNA in tumor tissues were significantly reduced in all medication groups （P<0.05）. Compared with the cisplatin group， the Dabufei decoction combined with cisplatin group showed significantly inhibited tumor growth， reduced tumor weight （P<0.05）， increased body weight （P<0.05）， increased spleen index and thymus index （P<0.05）， increased percentage of NK cells （P<0.05）， decreased percentage of Treg cells （P<0.05）， significantly increased counts of WBC， PLT， and HGB （P<0.05）， and reduced levels of phosphorylated PI3K， Akt， and mTOR and their mRNA （P<0.05）. ConclusionDabufei decoction combined with cisplatin has a synergistic effect with reduced toxicity， effectively regulating immune function， increasing the proportion of NK cells， reducing the proportion of Treg cells， improving bone marrow suppression， and downregulating the PI3K/Akt/mTOR signaling pathway to inhibit tumor growth in Lewis lung adenocarcinoma-bearing mice.
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ObjectiveTo explore the underlying mechanism by which the Chinese medicine compound Yitangkang granule（YTK） treats diabetic kidney disease （DKD） by observing its effects on podocyte autophagy through the regulation of phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/forkhead transcription factor O1 （FoxO1） signaling pathway mediated by silent information regulator 1 （SIRT1） via advanced glycation end products （AGE）/receptor for AGE （RAGE） axis. MethodNinety-six 8-week-old healthy male SPF-grade Wistar rats were selected and randomly divided into blank control group （B）， model control group， high-dose YTK （40 g·kg-1）， medium-dose YTK （20 g·kg-1）， low-dose YTK （10 g·kg-1）， and Western medicine control （20 mg·kg-1 losartan） groups. The DKD rat model was established by high-fat diet feeding combined with intraperitoneal injection of streptozotocin. After successful modeling， the rats in each group received the corresponding treatments for eight weeks. The levels of superoxide dismutase （SOD）， malondialdehyde （MDA）， glutathione peroxidase （GSH-Px）， and catalase （CAT） were measured according to the instructions of the respective assay kits. Hematoxylin and eosin （HE） staining was used to observe pathological changes in kidney tissues. Immunohistochemistry was employed to detect the average optical density values of α-smooth muscle actin （α-SMA）， fibronectin （FN）， desmin， and nephrin. Western blot analysis was used to measure the expression levels of PI3K， phosphorylated PI3K （p-PI3K）， Akt， phosphorylated Akt （p-Akt）， RAGE， SIRT1， Caspase-3， and FoxO1 proteins in kidney tissues of DKD rats. ResultCompared with the blank control group， the model group showed significantly lower levels of SOD， GSH-Px， and CAT， and significantly higher levels of MDA （P<0.01）. The rats exhibited severe kidney damage. The positive expression of podocyte marker proteins α-SMA， FN， and desmin increased significantly， while nephrin and podocin significantly decreased （P<0.01）. The expression levels of PI3K， p-PI3K， Akt， p-Akt， RAGE， and Caspase-3 proteins were significantly elevated， while SIRT1 and FoxO1 protein levels were significantly reduced （P<0.01）. Compared with the model control group， rats in the YTK treatment groups showed significantly higher levels of SOD， GSH-Px， and CAT， and significantly lower levels of MDA in serum （P<0.01）. The degree of kidney damage was reduced to varying extents. The average optical density values of podocyte marker proteins α-SMA， FN， and desmin were significantly decreased， while nephrin and podocin significantly increased （P<0.01）. The expression levels of PI3K， p-PI3K， Akt， p-Akt， RAGE， and Caspase-3 in kidney tissues were significantly reduced， while SIRT1 and FoxO1 expression levels significantly increased （P<0.01）. The Chinese medicine groups demonstrated a clear dose-response trend. ConclusionYTK may alleviate kidney pathological damage， reduce proteinuria， and protect kidney function in DKD rats， thereby delaying the progression of DKD by improving podocyte autophagy through the AGE-RAGE axis-mediated SIRT1 regulation of the PI3K/Akt/FoxO1 signaling pathway. Additionally， a dose-response relationship was observed in the Chinese medicine groups.
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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.
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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.
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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.
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Masculino , Animales , Ratas , Ratas Zucker , Proteínas Proto-Oncogénicas c-akt/genética , Diabetes Mellitus Tipo 2/terapia , Resistencia a la Insulina , Péptido C , Electroacupuntura , Hígado , Transducción de Señal , Insulina , LípidosRESUMEN
ObjectiveStudy on the mechanism of Guishao Yunpi decoction in preventing and treating breast hyperplasia based on phosphatase and tensin homolog （PTEN）/ phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） pathway. MethodSeventy SPF-grade SD rats were randomly assigned into blank group （n=15） and modeling group （n=55）. The mammary gland hyperplasia model of liver stagnation and spleen deficiency was established by the comprehensive modeling method （hunger and satiety abnormality + tail stimulation + estradiol benzoate + progesterone）， and then 5 rats were randomly selected for model verification. The modeled rats were then randomly assigned into five groups： model group， positive control （4 mg·kg-1·d-1 tamoxifen） group， and high-， medium-， and low-dose （17.2， 8.6， 4.3 g·kg-1·d-1， respectively） Guishao Yunpi decoction groups， with 10 rats in each group. The rats in the blank group and model group were given 10 mL·kg-1·d-1 distilled water， and those in other groups were orally administrated with corresponding drugs. After 30 days of treatment， the general living conditions of rats were observed， and the thickness of breast tissue was measured by an ultrasonic diagnostic instrument. The open field test was carried out for behavioral evaluation. The levels of B-cell lymphoma-2 （Bcl-2） and Bcl-2-associated X （Bax） in the breast tissue were determined by enzyme-linked immunosorbent assay （ELISA）. The mRNA and protein levels of PTEN， PI3K， and Akt in the breast tissue were determined by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot， respectively. ResultCompared with those in the blank group， the rats in the model group were irritable， curled up in clusters， and showed positive behavior in the open field test. The modeling led to nipple swelling and increased the breast thickness （P<0.05）. Moreover， the modeling elevated the level of Bcl-2 and lowered that of Bax in the breast tissue （P<0.05）， down-regulated the mRNA and protein levels of PTEN， and up-regulated the mRNA and protein levels of PI3K and Akt （P<0.05）. Compared with the model group， drug administration relieved the general survival state， the degree of nipple swelling， and the positive behavior in the open field test and reduced the breast thickness （P<0.05）. In addition， drug administration reduced the level of Bcl-2 and increased that of Bax in the breast tissue （P<0.05）， up-regulated the mRNA and protein levels of PTEN， and down-regulated the mRNA and protein levels of PI3K and Akt （P<0.05）. ConclusionGuishao Yunpi decoction can improve the general living conditions and alleviate the mammary gland hyperplasia of rats with the syndrome of liver depression and spleen deficiency， which may be realized by the regulation of the PTEN/PI3K/Akt pathway.
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Type 2 diabetes mellitus （T2DM） is a heterogeneous disease with insulin deficiency and insulin resistance （IR） as the main etiology and is often accompanied by complications. Volatile oil is a volatile oily liquid extracted from natural plants， which has many pharmacological effects such as regulating Qi， relieving pain， inhibiting bacteria， and reducing inflammation. In recent years， there have been numerous reports on the treatment of T2DM by natural plant volatile oil and its effective components， which has become one of the new directions in the treatment of T2DM. With natural plant essential oil and its active components as the starting point， this paper comprehensively analyzed and summarized the material basis， mechanism， and signaling pathways of essential oil in the treatment of T2DM and its complications in China and abroad in recent years， and focused on the inhibitory effect of essential oil and its active components， such as carvacrol， paeonol， and β-caryophylene， on IR to improve T2DM by protecting pancreatic β-cells， inhibiting α-glucosidase activity， regulating the abundance and diversity of intestinal microbiota， and regulating glucose transporter protein type4 （GLUT4）， adenylate 5′-monophosphate-activated protein kinase （AMPK）， phosphatidylinositol-3 kinase （PI3K）/protein kinase B （Akt） signaling pathways to provide some references for the volatile oil intervention in T2DM and the development of new green antidiabetic drugs.