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目的:研究熊果酸对乙醇所致小鼠急性酒精性肝损伤的保护作用及其机制。方法:将昆明种小鼠随机分为正常对照组、模型组、熊果酸组(15、30、60 mg/kg)及联苯双酯组(5.625 mg/kg)。每日灌胃给药1次,连续7 d。末次给药1 h后,除正常对照组外,分别灌胃给予50%乙醇14 ml/kg建立急性酒精性肝损伤模型。造模12 h后,处理动物,检测小鼠血清丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、γ-谷氨酰转移酶(GGT)和甘油三酯(TG)水平,以及肝组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)、谷胱甘肽(GSH)、肿瘤坏死因子-α(TNF-α)含量。苏木素-伊红(HE)染色,观察肝组织病理学变化。结果:与模型组比较,熊果酸组(15、30、60 mg/kg)均能明显降低血清中ALT、AST、GGT和TG水平以及肝组织中MDA、TNF-α含量,升高SOD活性和GSH含量。组织病理学显示,熊果酸可明显减轻小鼠肝损伤的病变程度。结论:熊果酸对乙醇所致的小鼠急性酒精性肝损伤具有保护作用,其机制可能与减轻脂质过氧化,抑制氧化应激以及炎症因子的过量释放,减轻炎症反应有关。
Objective: To study the protective effect of ursolic acid on alcohol-induced acute alcoholic liver injury in mice and its mechanism. Methods: Kunming mice were randomly divided into normal control group, model group, ursolic acid group (15, 30, 60 mg / kg) and bifendate group (5.625 mg / kg). Gavage administered once daily for 7 days. One hour after the last administration, except for the normal control group, 50% ethanol (14 ml / kg) was given intragastrically to establish acute alcoholic liver injury model. After 12 h of modeling, the animals were sacrificed and serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), γ-glutamyl transferase (GGT) and triglyceride ), And the activities of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH) and tumor necrosis factor-α (TNF-α) in liver tissue were measured. Hematoxylin - eosin (HE) staining, liver histopathological changes were observed. Results: Compared with the model group, the ursolic acid group (15,30,60 mg / kg) could significantly reduce the levels of ALT, AST, GGT and TG in the serum as well as the contents of MDA and TNF-α in the liver tissue, and increase the SOD activity And GSH content. Histopathology showed that ursolic acid can significantly reduce the severity of liver damage in mice. CONCLUSION: Ursolic acid has a protective effect on alcohol-induced acute alcoholic liver injury in mice. The mechanism may be related to the reduction of lipid peroxidation, inhibition of oxidative stress, excessive release of inflammatory cytokines and reduction of inflammatory reaction.