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目的:观察小牛血去蛋白提取物(DECB)对乙醇所致小鼠肝损伤的保护作用,并初步探讨其作用机制。方法:健康ICR小鼠60只,随机分为对照组、模型组、阳性药物组和低、中、高剂量DECB组,每组10只。腹腔灌胃给药,对照组小鼠给予生理盐水20mL·kg-1,低、中和高剂量DECB组小鼠分别给予0.125、0.250和0.500g·kg-1 DECB,阳性药物组小鼠给予护肝片0.63g·kg-1,每天1次,连续30d,末次给药1h后,除对照组外,其他各组小鼠一次性给予50%乙醇14mL·kg-1,并禁食16h建立急性酒精性肝损伤模型。测定小鼠的耐受酒精时间和醉酒时间,检测血清丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)活性,检测肝组织中甘油三酯(TG)、谷胱甘肽(GSH)和丙二醛(MDA)水平,并进行肝组织病理切片检查。结果:与模型组比较,各剂量DECB组小鼠醉酒症状明显减轻,高剂量DECB组和阳性药组小鼠酒精耐受时间延长(P<0.05),醉酒时间缩短(P<0.05),中、高剂量DECB组小鼠血清ALT和AST活性均明显降低(P<0.05)。与模型组比较,中、高剂量DECB组和阳性药物组小鼠肝组织中MDA和TG水平明显降低(P<0.05),GSH水平明显升高(P<0.05)。高剂量DECB组小鼠乙醇所致肝组织病理学损伤明显减轻。结论:DECB能明显改善乙醇所致肝损伤,其机制可能是通过抑制肝组织氧化应激反应实现的。
Objective: To observe the protective effect of deproteinized calf blood (DECB) on liver injury induced by ethanol in mice, and to explore its mechanism. Methods: Sixty healthy ICR mice were randomly divided into control group, model group, positive drug group and low, medium and high dose DECB group, 10 rats in each group. The mice in the control group were treated with saline 20mL · kg-1, and the mice in DECB group were given 0.125, 0.250 and 0.500g · kg-1 DECB respectively. The mice in the positive drug group were treated with DECB Liver slices 0.63g · kg-1, once a day for 30 days, the last administration of 1h, except for the control group, the other groups of mice given 50% ethanol 14mL · kg-1, and fasting 16h acute Alcoholic liver injury model. The tolerant alcohol time and drunk time of mice were measured. The activities of serum ALT and AST were measured. The contents of triglyceride (TG), glutathione Peptide (GSH) and malondialdehyde (MDA) levels, and liver biopsy. Results: Compared with the model group, the drunken symptoms of mice in DECB group were significantly reduced, the tolerance time of alcohol in DECB group and positive drug group were prolonged (P <0.05), the drunk time was shorter (P <0.05) Serum ALT and AST activities were significantly decreased in high-dose DECB mice (P <0.05). Compared with the model group, the levels of MDA and TG were significantly decreased (P <0.05) and the GSH levels were significantly increased in the middle and high dose DECB group and the positive drug group mice (P <0.05). High-dose DECB mice ethanol-induced liver tissue pathology damage was significantly reduced. Conclusion: DECB can significantly improve liver injury induced by ethanol, and its mechanism may be through the inhibition of oxidative stress in liver tissue.