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血管内皮生长因子在四氯化碳诱导的急性肝损伤小鼠肝组织中的表达 被引量:3

Expression of vascular endothelial growth factor in liver tissue of mice with acute liver injury induced by carbon tetrachloride
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摘要 目的观察四氯化碳(CCl4)诱导的急性肝损伤小鼠肝组织中血管内皮生长因子(VEGF)的表达。方法采用1 g.L-1 CCl4在小鼠腹部皮下注射建立急性肝损伤模型;分别在诱导后3、6、12、24、30、36、42、48、54 h,对肝组织石蜡切片采用苏木素-伊红染色法观察肝脏病理变化情况,采用赖氏法检测血清谷丙转氨酶(ALT)和谷草转氨酶(AST)活性变化,采用Western blot法检测VEGF蛋白表达。结果与阴性对照组相比,CCl4诱导后小鼠血清ALT、AST在不同时间点均显著升高(P<0.05),在36 h达到高峰,随后逐渐恢复到接近正常水平。小鼠肝脏组织结构在不同时间点均有不同程度受损,在36 h时组织受损最为严重。模型组小鼠VEGF蛋白表达量显著增加,24 h时达到高峰,随后逐渐降低。结论 CCl4诱导小鼠急性肝损伤过程中VEGF蛋白表达变化明显,VEGF在CCl4诱导的小鼠急性肝损伤过程中可能起重要作用。 Objective To investigate the expression of vascular endothelial growth factor(VEGF) in liver tissue of mice with acute liver injury induced by carbon tetrachloride(CCl4).Methods The mice models of acute liver injury were established by 1 g·L-1 CCl4 induced through the abdominal subcutaneous injection.The enzyme activities of ALT and AST in serum were analyzed and liver pathological changes were also observed by hematoxylin-eosin stain method at 3,6,12,24,30,36,42,48,54 hours after CCl4 injection respectively.The expressions of VEGF protein were determined by Western blot.Results Compared with the negative control group,the enzyme activity of ALT and AST were significantly increased(P0.05) in the model of liver injury at the different time,the highest level at 36 hours after CCl4 induced.The liver tissue structures were all harmed by CCl4 at the different level,especially at 36 hours,reached to the highest level.The expression of VEGF protein was significantly changed and reached the highest level at 24 hours and then gradually decreased to the normal level.Conclusion The expression of VEGF protein is significantly changed and probably plays an important role in the acute liver injury by CCl4.
出处 《新乡医学院学报》 CAS 2011年第3期268-271,共4页 Journal of Xinxiang Medical University
基金 国家自然科学基金资助项目(编号:30900796) 河南省高等学校青年骨干教师资助计划项目(编号:2010GGJS-074) 洛阳市科技攻关项目(编号:1001065A) 河南科技大学博士科研启动基金项目(编号:09001413)
关键词 四氯化碳 急性肝损伤 血管内皮生长因子 carbon tetrachloride acute liver injury vascular endothelial growth factor
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