Protective Effect Of Yulangsan Polysaccharide Against Hepatic Injury Induced By Diclofenac Sodium, Nimesulide And Ibuprofen In Mice

Objective： To observe the protective effect of Yulangsan Polysaecharide(YLSPS) on diclofenac sodium，nimesulide and ibuprofen-induced liver injuryin Kunming mice.Method：1.Animal and treatmentKunming mice were randomly divided into NC group，liver injured modelgroup with， high-，middle-，low-YLSPS group (600，300，150mg/kg) anddimethyl diphenyl bicarboxylate (200mg/kg DDB) group. The treatment groupswere orally administered once per day，whereas the normal and model groupswere orally administered with saline. Except normal mice, all the other micewere treated with drug induced liver injury for10days (nimesulide),14days(diclofenac, ibuprofen). At the end of the experimental period the mice were sacrificed and blood, liver samples were obtained.2.The indexs of the liver and spleen were observed3.Hematoxylineosin (HE) stain was used to examine the degree of hepaticinjury.4.Diclofenac sodium model：Estimation of ALT，AST and ALP, the content ofTBIL, TNF-α and IL-1β in serum and the activities of SOD, GSH–Px and CAT，the content of MDA in liver tissue. The levels of expression of Bax and Bcl-2mRNA in liver were examined by Real-time quantitative-PCR.5. Nimesulide model：Estimation of ALT，AST, ALP and T-AOC，the contentof TNF-α，IL-6in serum；the activities of SOD，GSH–Px and the content ofMDA in liver tissue. The expressions of Bax and Bcl-2in liver were detected byWestern Blot.6.Ibuprofen model：Estimation of of ALT，AST and ALP，the content ofT-AOC in serum；the activities of SOD，GSH-Px and the content of MDA inliver tissue were investigated. The expressions of Bax and Bcl-2in liver weredetected by immunohistochemical and Western Blot.Results：1.Diclofenac model： Compared with model group, YLSPS could obviouslyreduce the weight of the liver and spleen. The activities of ALT，AST andALP，the content of TBIL，MDA，TNF-α and IL-1β and the expression ofBax could be decreased. The activities of SOD，GSH-Px，CAT and theexpression of Bcl-2could be increased (P<0.05), and the degree of hepaticinjury could be lessened.2.Nimesulide model：Compared with model group， YLSPS could obviouslyreduce the activities of ALT，AST and ALP，the content of MDA，TNF-α， IL-6the index of liver, spleen and the expression of Bax. The activities ofSOD，GSH-Px，T-AOC and the expression of Bcl-2could be increased(P<0.05)；the degree of hepatic injury could be lessened.3.Ibuprofen model：Compared with model group，YLSPS could be decreasedthe index of liver and spleen，the activities of ALT，AST and ALP，the contentof MDA and the expression of Bax. The activities of SOD，GSH-Px，T-AOCand the expression of Bcl-2could be increased (P<0.05); the degree of hepaticinjury could be lessened.Conclusion：YLSPS has protective effect on diclofenac sodium, nimesulide andibuprofen-induced liver injury in mice. The mechanism may be related toattenuating free radical and inhibiting the effect on lipid peroxidation andapoptosis.