Objective: To investigate the signal transduction mechanism of leptin and the intervention effect of quercetin on the regulation of liver fibrosis in rats.
Method: Taking the CCl4-induced liver fibrosis rat model as the research object, 45 rats were randomly divided into 3 groups: control group, model group, and drug intervention group. The control group eats freely without any treatment. The model group and the visceral treatment group were intraperitoneally injected with 2 mL/kg 40?Cl4 vegetable oil solution twice a week for 8 weeks. On the 9th week of the experiment, rats in the treatment group were given 8 g/(kg?D) viscera by gavage, and rats in the model group were given the same amount of normal saline by gavage for 8 weeks. On the 17th week of the experiment, all animals were sacrificed by cervical dislocation and the left anterior lobe of the liver was excised. HE staining and MASSON staining were used to observe the effect of quercetin on the morphology of liver tissue in rats with liver fibrosis. Using immunohistochemical methods, we observed the effects of quercetin on leptin and leptin receptors in rat hepatic 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.
Results: The results of liver gloss, HE staining, and Masson collagen staining indicate that the rat liver fibrosis model is replicated normally, and quercetin has the effect of blocking and reversing liver fibrosis. Immunohistochemical staining showed that, compared with the model group, mistletoe alkaloids can significantly inhibit the expression of leptin and leptin receptor in the liver tissue of model rats. WesternBlot showed that the expression of JAK2 and STAT3 protein in the normal control group was the lowest, the expression of JAK2 and STAT3 protein in the model group was higher, while the expression of JAK2 and STAT3 protein in the drug treatment group was significantly reduced. It is regulated.
Conclusion: Mistletoe alkali can effectively reverse liver fibrosis in rats, and its mechanism is through down-regulating the expression of leptin and leptin receptors in rat liver tissues, and JAK2./STAT3 may affect the signal pathway.