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Chinese Journal of Comparative Medicine ; (6): 1-6, 2015.
Article in Chinese | WPRIM | ID: wpr-481395

ABSTRACT

Objective To investigate the signal transduction pathway mechanisms of rats with liver fibrosis regulated by leptin and interfering effects of mistletoe alkali .Methods The hepatic fibrosis in rats model was established by injecting carbon tetrachloride .Forty-five SD rats were randomly divided into normal group ,model group and therapeutic group.All rats except rats in normal group were intraperitoneally injected with 40%carbon tetrachloride in peanut oil with a dose of 2.0 mL/100g according to the body weight twice a week for 8 weeks.Then, the therapeutic group was given mistletoe alkali (8g/(kg· d)) for 8 weeks via gastrogavage.Rats in normal and model group were served with distilled water at the same time.At the end of the 16th week, blood and tissue specimens were taken from all the rats .The influence of mistletoe alkali on liver morphology in liver fibrosis rat model was reviewed by HE and Masson staining .The effects of mistletoe alkali on the expression of Leptin and its receptor ( OB-Rb ) in HSC in fibrosis rat model were determined by immunohistochemistry (IH).The expression of JAK2, STAT3 and the activity of phospho -JAK2, phospho-STAT3 were detected by Western blotting analysis .Results The degree of fibrosis of the model group was more severe than the normal group and the treatment group , which suggested that mistletoe alkali can reverse liver fibrosis in rats . Immunohistochemical staining showed that mistletoe alkali reduced the hepatic expression of leptin and OB -Rb in rats with liver fibrosis in comparison with their expression in the model group .Compared with the normal group , the expression of JAK2 and STAT3 increased in the model group .However, the expression of JAK2 and STAT3 decreased in the medication groups compared with the model group .Conclusion Mistletoe alkali can effectively ameliorate liver fibrosis in rats possibly through inhibiting hepatic leptin and its receptor expressions , which through inhibiting hepatic leptin and its receptor expressions , thus inhibit the JAK2/STAT3 signaling pathway .

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