库页红景天提取物对刀豆蛋白A诱导的小鼠免疫性肝损伤的保护作用

Protective effects of the extract of Rhodiola sachalinensis A.Bor.on immunologic liver injury induced by concanavalin A in mice

[目的]探讨库页红景天乙醇提取物对刀豆蛋白A(Con A)诱导的小鼠免疫性肝损伤的保护作用.[方法]取昆明种雄性小鼠,随机分为空白对照组、模型对照组和库页红景天提取物高、低剂量(1.0,0.5g/kg)组.库页红景天提取物高、低剂量组每日灌胃给予相应剂量的库页红景天提取物,连续7d.末次给药1h后,模型对照组、库页红景天提取物高、低剂量组均尾静脉注射给予Con A溶液18mg/kg.8h后采集血液,收集肝脏,测定各组血清AST,ALT,TNF-α,IL-6,IFN-γ和IL-4水平及肝脏MDA,GSH,SOD水平,并观察肝组织病理变化.[结果]与模型对照组比较,库页红景天提取物高、低剂量组肝脏指数、血清ALT水平及肝组织MDA含量均明显降低(P<0.05,P<0.01),肝脏GSH,SOD水平均明显升高(P<0.05,P<0.01),血清TNF-α,IL-6,IFN-γ和IL-4水平均明显降低(P<0.05,P<0.01),库页红景天提取物高剂量组AST活性明显降低(P<0.05).[结论]库页红景天乙醇提取物对Con A诱导的小鼠免疫性肝损伤具有保护作用.

OBJECTIVE To study the protective effects of ethanol extract of Rhodiola sachalinensis A.Bor.on immunologic liver injury induced by concanavalin A(Con A)in mice.METHODS The Kunming male mice were randomly divided into control group,model group,low and high dose of R.sachalinensis A.Bor.ethanol extract groups(0.5,1.0g/kg).The mice in the high and low dose groups were given R.sachalinensis A.Bor.ethanol extract by gavage for 7 days.One hour after the last administration,the mice in the model and the high and low dose groups were given Con A(18mg/kg)via tail intravenous injection.The blood and liver were collected after eight hours.The levels of AST,ALT,TNF-α,IL-6,IFN-γand IL-4 in serum were determined,the activities of MDA,GSH and SOD in liver tissue were measured,and the pathological changes of liver tissue were observed.RESULTSCompared with the model group,the liver index,the level of ALT in serum and the content of MDA in liver tissue were significantly decreased(P<0.05,P<0.01),the levels of GSH and SOD in liver tissue were significantly increased(P<0.05,P<0.01),and the levels of TNF-α,IL-6,IFN-γand IL-4 in serum were significantly reduced(P<0.05,P<0.01)in the high and low dose groups,while the activity of AST was significantly decreased in the high dose group(P<0.05).CONCLUSIONThe ethanol extract of R. sachalinensis A. Bor. had aprotective effect on immunologic liver injury induced by Con A in mice.