动物造模,小鼠慢性肝损伤 z-bio 2021-11-02 319

　　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.

　　Method Normal BALB/c mice were raised for 1 week and injected 0.5% CCL4 solution (10μL/g, 1 time/3 days for 10 weeks) into the intraperitoneal cavity. After the second, fourth, sixth, eighth, and tenth weeks of injection, the mouse serum was taken to detect ALT and AST. At the same time, the liver was fixed and stained with HE and Masson to observe the changes in the liver injury of the mice.

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

　　Conclusion Low-dose CCL4 induces chronic liver injury in mice with obvious and regular liver injury cycle changes. In the same cycle, the sequence of "injury, necrosis, regeneration, and repair" alternately dominates the pathological changes of liver tissue; for different research directions, it should be selected Corresponding "window period" conducts the mechanism research and drug efficacy evaluation of liver damage or repair.