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1.
Med Sci Monit ; 26: e923934, 2020 Aug 05.
Article in English | MEDLINE | ID: mdl-32756534

ABSTRACT

BACKGROUND Esophageal carcinoma (ESCA) is a health challenge with poor prognosis and limited treatment options. Our aim is to screen for hub genes and pathways associated with ESCA pathology as diagnostic or therapeutic targets. MATERIAL AND METHODS We downloaded 2 ESCA-related datasets from the Gene Expression Omnibus (GEO) database. Subsequently, differentially expressed genes (DEGs) of ESCA were determined by statistical analysis. Both Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of DEGs were performed using online analytic tools. Network analysis was employed to construct a protein-protein interaction (PPI) network and to filter hub genes. We evaluated the expression level and impact of hub genes on survival of ESCA patients using the OncoLoc webserver. RESULTS A total of 210 DEGs were identified. The GO analysis showed that the DEGs were enriched in cell division. The KEGG pathway analysis showed DEGs that were enriched in cell cycle regulation, known cancer pathways, the PI3K-Akt signaling pathway, and the cGMP-PKG signaling pathway. The top 10 hub genes were markedly upregulated in ESCA tissue compared with normal esophageal tissue. Moreover, the expression level of the hub genes was different at different pathological stages of ESCA. Further prognostic analysis identified that the top 10 hub genes were related to late survival of ESCA patients, while exhibiting few associations with early survival time. CONCLUSIONS The signaling pathways involving the DEGs probably represent the pathological mechanism underlying ESCA. The hub genes were associated with survival of ESCA patients, and as such have the potential to serve as diagnostic indicators and therapeutic targets.


Subject(s)
Adenocarcinoma/genetics , Adenocarcinoma/metabolism , Esophageal Neoplasms/genetics , Esophageal Neoplasms/metabolism , Esophageal Squamous Cell Carcinoma/genetics , Esophageal Squamous Cell Carcinoma/metabolism , Gene Regulatory Networks , Protein Interaction Maps/genetics , Adenocarcinoma/mortality , Biomarkers, Tumor/genetics , Biomarkers, Tumor/metabolism , Computational Biology/methods , Databases, Genetic , Esophageal Neoplasms/mortality , Esophageal Squamous Cell Carcinoma/mortality , Gene Expression Profiling , Gene Expression Regulation, Neoplastic , Gene Ontology , Humans , Phosphatidylinositol 3-Kinases/genetics , Phosphatidylinositol 3-Kinases/metabolism , Prognosis , Protein Interaction Mapping , Proto-Oncogene Proteins c-akt/genetics , Proto-Oncogene Proteins c-akt/metabolism , Signal Transduction/genetics , Survival Rate , Transcriptome
2.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-872432

ABSTRACT

Objective: To observe the effects of electroacupuncture (EA) on uterine prostaglandin F2α (PGF2α), cyclooxygenase 2 (COX-2) and nuclear factor κB (NF-κB) in rats with primary dysmenorrhea (PD) and to discuss the possible mechanism in EA intervening PD. Methods: Forty Sprague-Dawley female rats were randomly divided into a blank group, a model group, an EA group and an ibuprofen group, with 10 rats in each group. The PD model was established using estradiol benzoate combined with oxytocin in the model group, EA group and ibuprofen group. At the same time of modeling, rats in the EA group were given EA at Guanyuan (CV 4) and Sanyinjiao (SP 6) once a day for 20 min each time for 10 consecutive days. Ibuprofen was intragastrically administered once a day for 10 consecutive days in the ibuprofen group. The same amount of normal saline was intragastrically administered once a day for 10 consecutive days in the blank group and model group. The number of writhing of rats in each group within 30 min was compared on the 11th day just after the interventions. The uterine homogenate supernatant was separated and the PGF2α level was detected by enzyme-linked immunosorbent assay. Western blot was applied for the detection of the expression levels of COX-2, phospho-NF-κB p65 and NF-κB p65 proteins in uterine tissues. Results: Compared with the blank group, the number of writhing in the model group increased significantly (P<0.01), and the expression levels of PGF2α, COX-2, phospho-NF-κB p65 and NF-κB p65 proteins in uterine tissues were significantly increased (all P<0.01). Compared with the model group, the number of writhing in the EA group and ibuprofen group were significantly reduced (both P<0.01), and the expression levels of PGF2α and COX-2 protein in uterine tissues were significantly reduced (both P<0.01). Compared with the model group, the phospho-NF-κB p65 level in uterine tissues in the EA group was significantly reduced (P<0.01). Compared with the ibuprofen group, the phospho-NF-κB p65 level in the EA group was significantly reduced (P<0.01). Conclusion: The mechanism of EA for PD rats may be related to inhibiting the phosphorylation of NF-κB and reducing the levels of COX-2 and PGF2α in uterine tissues.

3.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-846704

ABSTRACT

Objective: To research the effects of astragaloside IV (AST IV) on improving insulin resistance in HepG2 cells, and predict and verify the AST IV possible targets based on pharmacophore model matching and molecular docking. Methods: HepG2 cells insulin resistance model was induced with high concentration insulin. After being interfered by AST IV, the glucose consumption was characterized by glucose test, AST IV possible targets were predicted by pharmacophore model matching and molecular docking, the expressions of related pathway protein were detected by Western blotting. Results: AST IV significantly increased the glucose consumption in insulin-resistant HepG2 cells, the possible target of AST IV may be related to tyrosine phosphotase 1B (PTP1B) based on pharmacophore model matching and molecular docking. The Western blotting results showed that, the level of PTP1B was significantly increased and the levels of p-IR and p-IRS-1 were significantly decreased in insulin-resistant HepG2 cells. The intervention of AST IV decreased the levels of PTP1B, and increased the levels of p-IR and p-IRS-1. Conclusion: AST IV can significantly improve insulin resistance of insulin induced HepG2 cells, and its mechanism is related to inhibiting PTP1B and activating insulin signaling pathways.

4.
Acupuncture Research ; (6): 548-551, 2020.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-844136

ABSTRACT

OBJECTIVE: To observe the effect of acupoint catgut embedding on levels of prostaglandin F2α(PGF2α), cyclooxygenase-2(COX-2) and nuclear factor kappa B(NF-κB) in the uteruses of rats with primary dysmenorrhea (PD), so as to explore its mechanisms underlying improvement of PD. METHODS: Forty female SD rats were randomly divided into normal, model, acupoint catgut embedment and medication groups, with 10 rats in each group. The PD model was established by subcutaneous injection of estradiol benzoate (0.5 mg on the 1st day, and 0.2 mg thereafter) once daily for 10 days, followed by i.p. of oxytocin 2 U(0.5 mg•5 U-1•mL-1) on the 11th day. Catgut embedment was applied to "Guanyuan"(CV4) and "Sanyinjiao"(SP6) on day 1 and 5 while modeling, and rats of the medication group received gavage of ibuprofen (1.25 mg/mL, 0.8 mL/rat) once daily for 10 d. The level of PGF2αin the uterus tissuewas assayed by ELISA, and the expression levels of uterine COX-2, phospho (p)-NF-κB p65, NF-κB p65 proteins were detected by Western blot. RESULTS: Compared with the normal group, the levels of PGF2α, COX-2, p-NF-κB p65 and NF-κB p65 in the uterine tissues were significantly increased in the model group (P<0.05). Compared with the model group, the levels of PGF2α and COX-2 in both catgut embedment and medication groups as well as p-NF-κB p65 in the catgut embedment group were significantly decreased (P<0.05). Compared with the medication group, the level of p-NF-κB 65 in the catgut embedment group was significantly decreased (P<0.05). CONCLUSION: The analgesic effect of acupoint catgut embedding may be related to its effects in down-regulating the expression of p-NF-κB and the levels of COX-2 and PGF2αin uteruses of PD rats.

5.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-878393

ABSTRACT

OBJECTIVE@#A study was conducted to systematically evaluate the clinical efficacy of inflammatory factors in patients with chronic kidney disease and periodontitis after non-surgical periodontal therapy.@*METHODS@#We searched the databases of CNKI, Wanfang, CBM, PubMed, Embase, and Cochrane Library from inception to December 2019. Two reviewers independently collected all literature related to inflammatory factors in patients with chronic kidney disease and periodontitis after non-surgical periodontal therapy. These factors include C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). The literature was screened according to the inclusion and exclusion criteria. The quality of the studies was strictly evaluated, and the data were extracted. The literature of randomized controlled trials in accordance with the standards was Meta-analyzed with Revman 5.3 software.@*RESULTS@#Six randomized controlled trials were included. Compared with the control groups, the results of meta-analysis showed that non-surgical periodontal therapy significantly reduced the levels of CRP [MD=-0.58, 95%CI (-1.13, -0.02), P=0.04] and IL-6 [MD=-2.76, 95%CI (-5.15, -0.37), P=0.02] in these patients but not that of TNF-α [MD=-3.87, 95%CI (-8.79, 1.05), P=0.12].@*CONCLUSIONS@#Simultaneous regular renal treatment and non-surgical periodontal therapy can help relieve the periodontal damage on patients with chronic kidney disease and periodontitis. Moreover, it can improve the status of some inflammatory factors. This finding is conducive to the control and treatment of chronic kidney disease and periodontitis and needs to be a focus of research and in clinical operation.


Subject(s)
Humans , C-Reactive Protein , Chronic Periodontitis , Interleukin-6 , Renal Insufficiency, Chronic/therapy , Tumor Necrosis Factor-alpha
6.
Acta Physiologica Sinica ; (6): 424-430, 2019.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-777171

ABSTRACT

The present study was aimed to investigate the protective effect and anti-inflammation mechanism of astragaloside IV (AST-IV) on cerebral ischemia and reperfusion injury. Following the establishment of cerebral ischemia and reperfusion model in rats by modified suture method, neurological deficit scores and cerebral infarct volume were used to evaluate the pharmacological effect of AST-IV against cerebral ischemia-reperfusion injury. Western blot was used to detect the expression levels of NLRP3, pro-Caspase-1, Caspase-1, pro-IL-1β, IL-1β, pro-IL-18, IL-18, phosphorylated and total nuclear factor kappa B (NF-κB)/p65 protein in the brain tissue. The results showed that compared with model group, the intervention of AST-IV decreased the neurological deficit scores, reduced the cerebral infarct volume, decreased the levels of NLRP3, Caspase-1, pro-IL-1β, IL-1β, pro-IL-18 and IL-18, and inhibited the expression of phosphorylated NF-κB in brain tissue. The results suggest that AST-IV has a protective effect against cerebral ischemia and reperfusion injury, and its mechanism is related to inhibiting the phosphorylation of NF-κB and NLRP3 inflammasome activation.


Subject(s)
Animals , Rats , Brain Ischemia , Drug Therapy , Infarction, Middle Cerebral Artery , Drug Therapy , Inflammasomes , Metabolism , NF-kappa B , Metabolism , NLR Family, Pyrin Domain-Containing 3 Protein , Metabolism , Phosphorylation , Rats, Sprague-Dawley , Reperfusion Injury , Drug Therapy , Saponins , Pharmacology , Triterpenes , Pharmacology
7.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-671628

ABSTRACT

As the main part of the teaching activities,students play an important role in the teaching reform.The students were trained through 3 pathways,“Extending teaching activities from the classroom to the outside”,“Development from basic to clinical knoledge” and “Culturing students' innovative consciousness”,so as to allow them to give full play in teaching reform,to enhance their ability of practice and learning by themselves,to culture their innovative consciousness and to develop students' leading functions in the anatomy teaching reform.

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