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目的探索本米[α-(2,4-二氯苯基)-咪唑-1-乙醇]对可卡因所致急性肝损伤的保护作用。方法 ICR雄性小鼠,体重18～22 g,按体重随机分为5组,每组10只。小鼠皮下注射可卡因制备急性肝损伤模型,采用治疗性给药方法,经口给予本米观察其保护作用。测定血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)和乳酸脱氢酶(LDH)活性,留取肝组织测定还原性谷胱甘肽(GSH)与氧化性谷胱甘肽(GSSG)的含量及比值,以及丙二醛(MDA)的含量,留取肝组织进行组织病理观察。结果与对照组相比,单独给予可卡因,血清中ALT、AST和LDH活性明显升高,肝组织中GSH/GSSG比值下降,MDA含量增加,肝小叶中心出现大量坏死细胞。与可卡因组相比,治疗性给予本米能明显降低血清ALT、AST和LDH活性,使肝组织中GSH/GSSG比值升高,MDA含量下降,肝小叶中心变性坏死细胞减少,坏死区域缩小。结论本米能够对可卡因引起的肝损伤起到保护作用,其机制可能是改善肝脏内的氧化应激环境。
Objective To explore the protective effect of Benmi [α- (2,4-dichlorophenyl) -imidazole-1-ethanol] against cocaine-induced acute liver injury. Methods ICR male mice weighing 18-22 g were randomly divided into 5 groups according to body weight, with 10 mice in each group. Mice were subcutaneously injected with cocaine to prepare a model of acute liver injury, and the therapeutic effect was obtained by oral administration of Benmi. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) activity were measured. Liver samples were collected for the determination of reducing glutathione (GSH) and oxidized glutathione (GSSG) content and ratio, as well as the content of malondialdehyde (MDA), liver tissue was collected for histopathological observation. Results Compared with the control group, cocaine alone was given. The activities of ALT, AST and LDH in serum were significantly increased, the ratio of GSH / GSSG in liver tissue was decreased, the content of MDA was increased and a large number of necrotic cells appeared in the center of hepatic lobule. Compared with the cocaine group, the therapeutic administration of Benmi significantly reduced the activities of serum ALT, AST and LDH, increased the ratio of GSH / GSSG in the liver tissue, reduced the content of MDA, decreased the denatured and necrotic cells in the hepatic lobule center and narrowed the necrotic area. Conclusions Benmi can protect cocaine-induced liver injury, and its mechanism may be to improve the oxidative stress environment in the liver.