动物造模,慢性肝损伤 z-bio 2022-10-06 620

　　Objective To study the characteristics of liver injury in a mouse model of chronic liver disease induced by carbon tetroxide (CCL4), and to explore its application in medical research.

　　Methods Normal BALB/c mice were routinely fed for 1 week and then intraperitoneally injected with 0.5% CCL4 solution (10 μL/g, once/3 days for 10 weeks). After the 2nd, 4th, 6th, 8th and 10th weeks of injection, the serum of the mice was collected to detect ALT and AST, and the liver was fixed and then stained with HE and Masson to observe the changes of liver damage in the mice.

　　Results When CCL4 solution was injected for 2 weeks, hepatocyte damage was mainly degeneration, with a large number of inflammatory cell infiltration and a small amount of collagen deposition, and ALT and AST were slightly increased; at 4 weeks, hepatocyte damage was mainly necrosis (P< 0.01), the number of hepatocytes (P<0.01) and inflammatory cell infiltration were decreased (P<0.01), collagen deposition developed into cord-like collagen fiber deposition, and ALT and AST increased significantly (P<0.01); 6 At week 2, the necrosis of hepatocytes was significantly decreased (P<0.01), the number of hepatocytes was relatively increased (P<0.01), the infiltration of inflammatory cells was also decreased (P<0.01), and the deposition of collagen fibers was transformed into deposition of collagen (P<005). ), ALT and AST were basically normal; at 8 weeks, the degeneration of liver cells increased again, accompanied by a large number of inflammatory cell infiltration (P<0.01), and ALT and AST were slightly increased; at 10 weeks, liver cell damage was mainly necrosis again (P<0.01), the number of hepatocytes (P<0.01) and the infiltration of inflammatory cells were decreased (P<0.05), the collagen deposition developed into cord-like collagen fiber deposition, and ALT and AST were significantly increased (P<0.01). .

　　Conclusion Low-dose CCL4-induced chronic liver injury in mice has obvious and regular cyclic changes in liver injury. In the same cycle, the sequence of "injury, necrosis, regeneration, and repair" alternately dominates the pathological changes of liver tissue. In the corresponding "window period", the mechanism research and drug efficacy evaluation of liver injury or repair are carried out.