动物造模,非酒精性脂肪肝 z-bio 2023-04-21 460

　　Objective: To investigate the role of mitochondria-cytochrome C pathway in the apoptosis of rabbit non-alcoholic fatty liver liver cells.

　　Methods: Forty male Japanese rabbits were randomly divided into normal control group (8 weeks) and NAFLD model group (4, 6, and 8 week groups), 10 in each group. The model group was subcutaneously injected with peanut oil at 1.2 mL/kg, twice a week, to establish a Japanese big-eared rabbit model of NAFLD. The rabbits were sacrificed according to the time points of each group, and the levels of biochemical indexes in the serum of the rabbits were determined; the pathological changes of liver tissue were observed by HE staining, and the apoptosis rate of hepatocytes was detected by flow cytometry; liver mitochondria were extracted, and the mitochondrial permeability transition pores were detected by spectrophotometry ( The state changes of mitochondrial permeability transition pore, MPTP); the expressions of Bcl-2, Bax, cytochrome C and caspase-3 in liver tissue were detected by immunohistochemistry; the changes of cytochrome C and caspase-3 contents were detected by Western blot.

　　Results: Compared with the normal control group, the expression levels of liver lipid metabolism indexes and related inflammatory factors in the model group were increased, and the apoptosis rate of hepatocytes in the model group was significantly increased compared with the control group (P<0.01). At 4 weeks after modeling, liver function damage and lipid metabolism disorder occurred. With the development of NAFLD, the expression levels of Bcl-2, Bax, cytochrome C and caspase-3 gradually increased, and the mitochondrial permeability transition pore opening rate increased with high lipid levels. The prolonged feeding time was significantly increased (P<0.01).

　　Conclusion: The mitochondria-cytochrome C pathway plays a certain regulatory role in NAFLD-induced hepatocyte apoptosis.