1. Knife bean protein A-induced liver injury model
[Operation steps] BALB/c mice, 15-20g, diluted with PBS to 2mg/ml of adzuki bean protein A, and injected via tail vein at 10-20mg/kg. Liver injury can occur after 8 hours.
【 Result Analysis 】 Knife bean protein A can activate CD8+or CD4+cells, increase the release of IFN - γ, which induces a comprehensive cytokine response by promoting the infiltration of inflammatory cells into the portal vein area and activating macrophage function, resulting in cytotoxic effects on liver cells. After 8 hours of administration, serum ALT and AST levels significantly increased, and pathological changes showed severe infiltration of neutrophils, lymphocytes, and monocytes in the liver lobules. Inflammatory lesions were also visible in the portal vein and central vein areas, and electron microscopy showed diffuse hepatocyte necrosis.
2. Liver injury model induced by delayed hypersensitivity mechanism induced by picryl chloride (PCL)
【 Operation steps 】 BALB/c, ICR, or Kunming mice, weighing 15-20g, were sensitized by applying 0.1ml of 1% PCL ethanol solution to the abdomen of pre shaved mice. After 5 days of sensitization, the sensitization was repeated. After 5 days of the second sensitization, 10 μ l of 0.2% -0.5% PCL olive oil solution was injected into the liver for attack. The results could be observed after 18 hours.
【 Result Analysis 】 The main reactive cells of delayed hypersensitivity reactions are Th1 type lymphocytes and their chemotactic inflammatory cells. Bitter nitrogen can activate immune mediated immune damage caused by Th1 type lymphocytes. The pathological manifestations of the model include significant elevation of ALT and AST, hepatocyte necrosis, and infiltration of inflammatory cells in the portal area. The degree of this liver damage is directly proportional to the intensity of the immune response, and this damage is not limited to the injection site and can spread throughout the entire liver.