Protective Effects And Mechanisms Of YLS On Chemical Liver Injury

Objective: To study the protective effects and mechanisms of YLS on Cd4, thioacetamide (TAA) and acetaminophen (AP) -induced acute liver injuiy in mice and CCh-induced chronic liver injuiy in Wistar rats. Methods: The models of CC!4, TAA and AP- induced acute liver injury in mice and CC!4- induced chronic liver injury in Wistar rats were used to study the protective effects and its involved mechanisms of YLS on liver injury. The effects of YLS on free radicals of superoxide anion (Or) and hydroxy( OH) were investigated by the method of speclrophotometry (wave length 322nm and 536nm). Results: YLS could significantly decrease the elevation of serum transaminase in liver injuries induced by CCLI, TAA and AP in mice (P-ATPase and glutathione peroxidase (GSH-PX) and the contents of glutathione (GSH) in both serum and liver were markedly increased by the treatment with YLS. YLS could also markedly decrease the content elevation of hydroxyproline (HYP) in liver, increase the content of total protein (UP) and albumin (ALB), and decrease the activities of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) in chronic liver injury induced by CC!4 in Wrstar rats. Other experiments showed that YLS had a great scavenging action of 0 and ?OH. Conclusion: YLS has the significant protective effects on CC!4, TAA and AP-induced acute liver injuries in mice and Cdtrinduced chronic liver injury in rats, possibly due to its antioxidaiive capability, and induction of hepatic microsomal drug metabolizing enzymes and inhibition of lipid peroxidation and Ca²⁺ overloading.