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目的:研究葫芦茶苷对四氯化碳(CCl4)诱导急性肝损伤大鼠的保护作用及对肝组织Caspase-3与Caspase-8活性的影响。方法:将健康雄性SD大鼠随机分为正常对照组,肝损伤模型组,阳性对照组(水飞蓟宾胶囊),葫芦茶苷低中高剂量组(3、6、12 mg·kg-1),每日灌胃给药1次,连续给药14 d,正常组与模型组每天灌服等体积的生理盐水,末次灌胃给药1 h后,除空白对照组外,皮下注射CCl4原液建立急性肝损伤大鼠模型,检测大鼠血清丙氨酸氨基转移酶(ALT)、门冬氨酸氨基转移酶(AST)、乳酸脱氢酶(LDH)和γ-氨基酰转肽酶(γ-GT)、胆碱酯酶(CHE)、总胆汁酸(TBA)和总胆红素(TBIL);检测肝组织匀浆超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)活性以及还原型谷胱甘肽(GSH)、丙二醛(MDA)和肝微粒体一氧化氮(NO)的含量,并检测肝组织Caspase-3,Caspase-8活性。结果:与模型组比较,葫芦茶苷能降低血清ALT,AST,LDH,γ-GT活性及TBA和TBIL含量(P<0.05或P<0.01),升高血清CHE含量;降低肝微粒体NO含量和MDA含量,增加肝组织SOD,GSH-PX活性和GSH含量,并降低肝组织Caspase-3,Caspase-8的活性(P<0.05或P<0.01)。结论:葫芦茶苷对四氯化碳致急性肝损伤大鼠具有明显的保护作用,其机制可能与其抗氧自由基、抑制脂质过氧化作用以及下调Caspase-3和Caspase-8的活性有关。
Objective: To study the protective effect of gourdin on CCl4-induced acute liver injury in rats and its effect on the activity of Caspase-3 and Caspase-8 in liver tissue. Methods: Healthy male Sprague-Dawley rats were randomly divided into normal control group, liver injury model group, positive control group (silybin capsule), low and medium dose of gourdin group (3, 6, 12 mg · kg- The rats in the normal group and model group were fed with the same volume of normal saline daily for 1 h. The control group was injected subcutaneously with CCl4 stock solution Acute liver injury rat model was used to detect serum ALT, AST, LDH and γ- GT, CHE, TBA and TBIL. The levels of superoxide dismutase (SOD), glutathione peroxidase (GSH) -PX activity and the content of glutathione (GSH), malondialdehyde (MDA) and liver microsomal nitric oxide (NO) in liver tissue were determined. The activities of Caspase-3 and Caspase-8 in liver tissue were detected. Results: Compared with model group, gourdin reduced serum ALT, AST, LDH, γ-GT activity and TBA and TBIL contents (P <0.05 or P <0.01), increased serum CHE content and decreased liver microsomal NO content (P <0.05 or P <0.01). The levels of SOD, GSH-PX and GSH in the liver tissue were significantly increased and the activities of Caspase-3 and Caspase-8 in liver tissue were decreased. CONCLUSION: Hulululose has a protective effect on carbon tetrachloride-induced acute liver injury in rats. The mechanism may be related to the antioxidant activity of free radicals, the inhibition of lipid peroxidation and the down-regulation of Caspase-3 and Caspase-8.