[Animal Modeling]-Liver Fibrosis Model

  Objective: To explore whether iron can promote the process of liver fibrosis in rats.

  Method: The rats were divided into control group, high-fat group, high-speed iron group, high-fat high-iron group, high-fat iron removal group, 24 animals in each group. Rats in the high-iron and high-fat and high-iron groups were injected intramuscularly with 50 mg/kg iron dextran every other day. Rats in the high-fat deironing group received intravenous injection of iron methanesulfonate for 1 month. Before the sacrifice. Ammonium salt 30 mg/kg, 3 times a week, 8 rats were selected under the intervention of 4, 5 and 6 months to detect hyaluronic acid (HA), type IV collagen (type IV collagen, COL-IV) ). Laminin (LN), procollagen III (PCIII); Masson staining is used to observe the pathological changes of the liver.

  Results: 5 months after the intervention, the HA levels of the high-fat and high-iron groups were higher than those of the control and high-fat groups; the COL-IV levels and LN levels of the high-fat and LN groups were 6-high-fat groups were higher than the high-fat groups. 6 months after the intervention, the high-fat group was the high-fat diet group, and the high-fat group was the serum PCⅢ level. Masson staining of liver specimens in the high-fat and high-iron groups showed significant collagen deposition, while the other groups had no collagen deposition.

  Conclusion: Iron may accelerate the process of liver fibrosis in rats caused by hyperlipidemia.