高活性小牛血去蛋白提取物对四氯化碳致急性肝损伤模型小鼠的保护作用

发布时间：2019-04-03 11:50

【摘要】：目的:观察小牛血去蛋白提取物(DECB)对四氯化碳(CCl_4)所致肝损伤小鼠的保护作用,初步探讨其作用机制。方法:健康ICR种小鼠40只,随机分组法分为对照组、模型组、DECB组和阳性药物组,每组10只。各组小鼠腹腔灌胃给药,对照组和模型组小鼠给予生理盐水20mL·kg~(-1),DECB组小鼠给予DECB1g·kg~(-1),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2h后,对照组小鼠腹腔注射调和油溶液,其余各组小鼠腹腔注射10%CCl_4调和油溶液(10mL·kg~(-1))并禁食,建立CCl_4致急性肝损伤模型。测定各组小鼠血清中丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)活性和肝组织总超氧化物歧化酶(T-SOD)、谷胱甘肽(GSH)及丙二醛(MDA)水平;HE染色法观察小鼠肝组织病理表现;TUNEL方法检测小鼠肝细胞凋亡。结果:与模型组比较,DECB组和阳性药物组小鼠血清中ALT和AST活性及肝组织中MDA和GSH水平明显降低(P0.05),T-SOD水平明显升高(P0.05);与模型组比较,DECB组和阳性药物组小鼠肝组织病理学损伤明显减轻,凋亡细胞数明显减少。结论:DECB对CCl_4诱导急性肝损伤小鼠具有保护作用,可以增强肝脏抗氧化能力,抑制肝细胞凋亡,其机制可能与减少氧自由基和抑制脂质过氧化有关。
[Abstract]:Objective: To observe the protective effect of DECB on the liver injury induced by carbon tetrachloride (CCl _ 4) and to explore its mechanism of action. Methods:40 healthy ICR mice were randomly divided into control group, model group, DECB group and positive drug group. In the control group and the model group, the mice were given 20 mL 路 kg ~ (-1) of normal saline, and the mice of the DECB group were given DECB1g 路 kg ~ (-1), and the mice of the positive drug group were given the protective liver pieces of 0.63 g 路 kg ~ (-1),1 time and 30 days each day, and after the last dose of 2 h, the control group mice were injected with the mixed oil solution. A 10% CCl _ 4 blend oil solution (10 mL 路 kg ~ (-1)) was injected intraperitoneally in the rest of the mice, and the acute liver injury model induced by CCl _ 4 was established. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total superoxide dismutase (T-SOD), glutathione (GSH) and malondialdehyde (MDA) in the liver of mice were determined by HE staining. TUNEL method was used to detect the apoptosis of mouse hepatocytes. Results: Compared with the model group, the activity of ALT and AST in the serum of the DECB group and the positive drug group and the level of MDA and GSH in the liver tissue were significantly lower (P0.05), and the level of T-SOD was significantly higher (P0.05). Compared with the model group, the pathological damage of liver tissue in the DECB group and the positive drug group was significantly reduced. The number of apoptotic cells was significantly reduced. Conclusion: The protective effect of DEECB on CCl _ 4 induced acute liver injury can enhance the anti-oxidation ability of the liver, inhibit the apoptosis of the liver cells, and the mechanism may be related to the reduction of oxygen free radicals and the inhibition of lipid peroxidation.
【作者单位】：北华大学药学院微生物与生化药学教研室;
【基金】：吉林省科技厅科技创新与科技成果转化计划基金资助课题(0150312014ZX);吉林省科技厅医药产业发展资金项目资助课题(20140311084YY) 吉林省卫计委科研项目资助课题(20142078) 吉林省发改委科研基金资助课题(2014Y103)
【分类号】：R965;R-332

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