Effects of genistein sodium sulfonate on liver function and liver tissueα7nAchR and IL-1βexpression in mice chronic hepatic injury / 重庆医学

ABSTRACT

Objective To observe the protective effects of genistein sodium sulfonate(GSS)on mice chronic hepatic injury in-duced by carbon tetrachloride(CCl4 )and its influence on the protein expression of α7 nicotinic acetylcholine receptor(α7nAChR) and interleukin-1 beta (IL-1β)in liver tissue.Methods 60 SPF grade male Kunming mice were randomly divided into 5 groups,in-cluding the control group,model group,low and high doses GSS groups,and positive control group,12 cases in each group.Except for the control group,the other 4 groups were intra peritoneally injected by 10 % CCl4 with a volume of 0.1 mL/10 g for 6 weeks. The mice chronic liver injury was prepared.At the same time,the high and low doses DSS groups were given the different doses of GSS(0.30,0.10 mg/kg),the positive control group was given bifendate(DDB,2.5mg/kg),the control group and the model group were given the equal volume of normal saline for 6 consecutive weeks.The AST and ALT activity was detect and the ratio of ALT/AST was calculated;the Western blot method was used to detect the expression levels ofα7nAChR and IL-1βprotein in liver.Re-sults The serum levels of ALT and AST in the model group were increased obviously,and the expression level ofα7nAChR in the liver tissue was decreased,while the expression level of IL-1βwas increased;after the GSS treatment,the serum AST and ALT lev-els were significantly lower than those in the model group(P <0.05),while the expression level ofα7nAChR was increased (P <0.01)and the expression level of IL-1βwas decreased(P <0.05).Conclusion GSS might increase the expression ofα7nAChR in injured liver tissue,activates the cholinergic anti-inflammatory pathway,thus decreases the expression of inflammatory cytokines and antagonizes the mice chronic liver injury by inhibiting the inflammatory reaction.