胱硫醚γ-裂解酶-硫化氢在脂多糖诱导大鼠肝细胞凋亡中的作用及机制的中期报告.docxVIP

胱硫醚γ-裂解酶-硫化氢在脂多糖诱导大鼠肝细胞凋亡中的作用及机制的中期报告 Abstract: The purpose of this study is to investigate the role and mechanism of cysteine ??thioesterase-γ (CTSG)-hydrogen sulfide (H2S) in lipopolysaccharide (LPS)-induced apoptosis of rat liver cells. The study used established in vitro cell models to simulate the effects of LPS on rat liver cells, and explored the effects of CTSG and H2S on the apoptotic process of liver cells. The results showed that the expression of CTSG and H2S in LPS-treated liver cells increased significantly compared with the untreated control group. Apoptotic cells were also significantly higher in the LPS-treated group than in the control group. However, when cells were treated with a CTSG inhibitor, the number of apoptotic cells decreased significantly. This suggests that CTSG plays an important role in LPS-induced apoptosis of liver cells. Further experiments showed that the mechanism of CTSG action in liver cell apoptosis may be related to the regulation of the p38 MAPK signaling pathway. The study found that LPS increased the expression of p38 MAPK in liver cells, which in turn led to an increase in CTSG expression. When the p38 MAPK signaling pathway was inhibited, the expression of CTSG was also reduced, and the number of apoptotic cells decreased. In conclusion, this study provides evidence that CTSG and H2S are involved in LPS-induced apoptosis of liver cells. The results suggest that CTSG regulates the apoptosis of liver cells by activating the p38 MAPK signaling pathway. These findings may provide new insights for the development of therapeutic strategies for liver diseases.