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The JAK/STAT/SOCS signaling pathway can mediate a variety of cytokines involved in inflammation, tumor, and autoimmune diseases and it also plays an important role in hepatitis B virus (HBV) infection-related liver diseases. This article briefly reviews the structure and signal pathway regulation of JAK-STAT and SOCS and elaborates on their role in the development and progression of HBV-related chronic hepatitis B, liver cirrhosis, liver failure, and hepatocellular carcinoma. The final analysis shows that the JAK/STAT/SOCS signaling pathway is dysregulated in HBV-related liver disease and is involved in the development and progression of the disease, and it may even influence the treatment and prognosis of the disease.
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Patients with chronic hepatitis B (CHB) often have immune-mediated liver injury, and it is considered that the interaction between viral infection and immune response is an important cause of disease progression. CHB can progress to liver fibrosis, liver cirrhosis, and even hepatocellular carcinoma (HCC). This article reviews the discovery of T helper 17 (Th17) cells and regulatory T (Treg) cells, describes their own features, and elaborates on their role and mechanism of action in maintaining the stability of the immune system. This article also analyzes the role of Th17/Treg cell imbalance in CHB, liver fibrosis, liver cirrhosis, and HCC and points out that Th17/Treg cell imbalance may promote the aggravation of HBV-related liver diseases.
RESUMO
Objective: To explore the effects of ramipril, trimetazidine and the combination of ramipril and trimetazidine on renal cell apoptosis index (AI) and cytochrome C (Cyt-C) expression in experimental rats with chronic heart failure (CHF). Methods: CHF model was established by partially banding of abdominal aorta superior to renal artery in experimental rats. A total of 50 male Wistar rats were randomly divided into 5 groups: Sham operation group, Model group, Ramipril group, Trimetazidine group and Combination (ramipril and trimetazidine) group.n=10 in each group. Renal tubular cell AI was examined by TUNEL method, mRNA and protein expressions of Cyt-C were detected by RT-PCR and Western Blot analysis in each group respectively. Results: Compared with Sham operation group, Model group had increased AI of renal tubular cells, increased mRNA and protein expressions of Cyt-C,P Conclusion: Ramipril and trimetazidine can inhibit renal cell apoptosis and effectively improve the renal function in CHF rats. Combined medication is better than either of them alone.