玉郎伞多糖对药物性肝损伤小鼠的保护作用

Protective Effect of Yulangsan Polysaccharide Against Hepatic Injury in Mice

目的探讨玉郎伞多糖对布洛芬(IBU)致小鼠肝损伤的保护作用及可能机制。方法将昆明种小鼠随机分成6组,每组10只,即空白对照组(NC),模型对照组,玉郎伞多糖大(600 mg·kg-1)、中(300 mg·kg-1)、小(150 mg·kg-1)剂量组及联苯双酯组(联苯双酯,150 mg·kg-1)。玉郎伞多糖大、中、小剂量组和联苯双酯组灌胃给予相应药物,每日1次,连续14 d。末次给药后2 h,除NC组外,其他各组一次性灌胃IBU,200 mg·kg-1,制备小鼠肝损伤模型。造模后禁食不禁水20 h,测定天冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)、总胆红素(T-Bi L)、碱性磷酸酶(ALP)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)及丙二醛(MDA)水平;取肝组织行病理学检查,观察肝组织损伤程度。结果与模型对照组比较,玉郎伞多糖各剂量组血清ALP、AST、ALT活性降低,T-Bi L及IL-6、TNF-α水平降低;肝组织MDA水平降低,肝匀浆SOD及GSH-Px水平升高(P<0.05)。玉郎伞多糖可减轻肝细胞损伤程度。结论玉郎伞多糖对IBU所致肝损伤小鼠具有保护作用,其机制可能与抗氧自由基损伤、抗脂质过氧化损伤及减少炎症因子释放等有关。

Objective To investigate the protective effect of Yulangsan polysacharide （ YLSPS） and mechanism against ibuprofen-induced liver injury in mice. Methods The mice were randomly divided into the blank control（NC）, the model control,YLSPS at 150 mg·kg-1 , 300 mg·kg-1 ,600 mg·kg-1 groups and biphenyldicarboxylate （150 mg·kg-1 BPDC） group. The mice were orally administered with corresponding agents once per day for consecutive 14 days, whereas the blank control group and model control group were orally administered with saline. Except the blank control group, all the other mice were orally administered IBU 200 mg·kg-1 body weight 2 h after last lavagedof medicimes. The mice were fasted and watered ad lib for 20 h after model establishment. Activities of ALT,AST and ALP,content of T-BiL,TNF-α,IL-6 in serum;activities of SOD,GSH-Px and content of MDA in liver tissue were detected. The morphological pathology test was used to examine degrees of hepatic injury. Results Compared with the model control, YLSPS could obviously reduce activities of ALT,AST and ALP,content of T-BiL, MDA,TNF-α and IL-6, and increase SOD,GSH-Px and CAT （P〈0. 05）, and then lessen the hepatic injury. Conclusion YLSPS showed potential protective effect against ibuprofen-induced liver injury in mice, the mechanism may be related to attenuating free radical injury and inhibiting lipid peroxidation and lowering release of inflammatory factors.