瘦素对大鼠肝纤维化 z-bo 2020-11-06 373

　　OBJECTIVE: To investigate the signal transduction mechanism of leptin in regulating liver fibrosis in rats and the intervention effect of quercetin.

　　Method: Taking the CCl4-induced liver fibrosis rat model as the research object, 45 rats were randomly divided into three groups, namely the control group, the model group, and the drug intervention group. The control group did not do any treatment and was free to eat and drink; the model group and the visceraline treatment group were intraperitoneally injected with 40% CCl4-vegetable oil solution 2 mL/kg, twice a week for 8 weeks. On the 9th week of the experiment, the rats in the treatment group were given 8g/(kg·d) of viscerine by gavage, and the model group was given the same dose of normal saline by gavage for 8 weeks. At the 17th week of the experiment, all animals were killed by cervical dislocation, and the left anterior lobe of the liver was taken out. HE staining and MASSON staining methods were used to observe the effect of quercetin on liver tissue morphology of hepatic fibrosis rats; immunohistochemical methods were used to observe the effect of quercetin on leptin and leptin receptor in rat liver stellate cells. Western Blot method was used to detect JAK2 and STAT3 protein levels and JAK2 and STAT3 protein phosphorylation levels in rat liver tissues.

　　Result: The liver gross, HE staining and Masson collagen staining results suggest that the rat liver fibrosis model is successfully replicated, and quercetin can block and reverse liver fibrosis. Immunohistochemical staining showed that, compared with the model group, mistletoe alkali significantly inhibited the expression of leptin and leptin receptor in the liver tissue of model rats. Western Blot showed that the expression of JAK2 and STAT3 protein in the normal control group was the least; the expression of JAK2 and STAT3 protein in the model group was high; while the expression of JAK2 and STAT3 protein in the drug treatment group was significantly down-regulated.

　　Conclusion: Mistletoe base can effectively reverse liver fibrosis in rats, and its mechanism of action may be accomplished by down-regulating the expression of leptin and leptin receptors in rat liver tissues, thereby affecting the JAK2/STAT3 signaling pathway.