动物实验,细胞色素C z-bo 2020-08-24 509

　　Objective: To investigate the role of mitochondrial cytochrome C pathway in hepatocyte apoptosis in rabbits with non-alcoholic fatty liver (NAFLD).

　　Method: 40 big-eared rabbits were randomly divided into normal control group (8 weeks) and NAFLD model group (4, 6, 8 weeks group), each with 10 rabbits. In the model group, 1.2 mL/kg peanut oil was injected subcutaneously twice a week to establish the NAFLD model of Japanese rabbits. According to the time point of each group, the rabbits were sacrificed, and their serum levels of biochemical indicators were determined. The pathological changes of liver tissues were observed by HE staining, and the apoptosis rate of liver cells was detected by flow cytometry. The liver mitochondria were extracted and the mitochondrial permeability transition pore (mitochondrial permeability transition pore, MPTP) was detected by spectrophotometry; the immunity confirmed the expression of Bcl-2, Bax, cytochrome C and caspase-3 in liver tissue. Histochemical method; Western blotting method to detect the changes of cytochrome C and caspase-3 content.

　　Result: Compared with the normal control group, the expression level of inflammatory factors related to lipid metabolism index in the liver of the model group increased, and the apoptosis rate of liver cells in the model group was significantly higher than that of the control group. It is increased to (P\u003c0.01). Liver dysfunction and abnormal lipid metabolism occurred within 4 weeks of modeling. With the development of NAFLD, the expression of Bcl-2, Bax, cytochrome C and caspase-3 gradually increased, and the opening rate of the mitochondrial permeability transition pore increased with high fat. Long-term feeding time is significantly increased (P\u003c0.01).

　　Conclusion: Mitochondrial cytochrome C pathway plays a specific regulatory role in NAFLD-induced hepatocyte apoptosis.