Protective Effects And Possible Mechanisms Of Total Glucosides Of Paeony On Acute Liver Injury

Objective To investigate the effects of total glucosides of paeony (TGP) on carbontetrachloride-induced chemical liver injury and Bacillus Calmette Guerin (BCG) pluslipopolysaccharide(LPS)-induced immunological liver injury in mice as well as itspossible mechanisms.Methods The model of chemical liver injury and immunological liver injury in mice was prepared. The levels of alanine aminotransferase(ALT), aspartate aminotransferase(AST) , nitric oxide(NO) in serum, malondiadehyde(MDA) content, superoxide dismutase(SOD) and glutathione peroxidase(GSH-px) activities in liver homogenate were assayed by spectrophotometry; Tumour necrosis factor- a (TNF- a ) activity was determined by ridio immunoassay method. ConA- and LPS- induced splenocytes proliferation was assayed by MTT dye reduction. Meanwhile, hepatic pathological examination was observed.Results 1 Protective effect of TGP on carbon tetrachloride-induced chemical liver injury: TGP (60, 120, 240mg kg-1) was able to significantly decrease serum transaminase (ALT, AST) levels of chemical liver injury's mice induced by carbon tetrachloride, attenuate the area and extent of necrosis and reduce the infiltration of inflammatory cells. Furthermore, TGP also decreased MDA content and improved the reduced SOD and GSH-px levels in liver homogenate.2 TGP (60, 120, 240mg kg-1) was able to significantly decrease serum transaminase (ALT, AST) levels of immunological liver injury's mice induced by BCG plus LPS, attenuate the area and extent of necrosis and reduce the infiltration of inflammatory cells. Furthermore, TGP also decreased MDA content and improved thereduced SOD and GSIl-px levels in liver homogenate. Meanwhile, TGP(60, 120, 240mg kg-1) significantly lowered increased TNF-a and TGP(I20, 240mg kg-1) lowered increased NO level in serum . TGP(60, 120, 24()mg kg-1) could reverse LPS or ConA-induced splenocyte proliferation response.Conclusion TGP possesses protective action on chemical liver injury and immunological liver injury in mice, which was related to direct with free radical scavenging, increasing the content of SOD and GSH-px, imtnunoloregtilation and so on.