COPD模型大鼠急性加重期诱导肝脏损害的实验研究  

Experimental Research on Inducing Hepatic Damage in the Course of the Acute Exacerbation of COPD Model Rats

作　　者：孙璐璐[1] 张伟[2] 韩佳[1] 姚玉强[1] 谷明明[1] 

机构地区：[1]山东中医药大学,山东济南250014 [2]山东中医药大学附属医院,山东济南250011

出　　处：《中医学报》2014年第3期334-337,共4页Acta Chinese Medicine

基　　金：山东省自然科学基金资助项目(编号:Y2006C114);"泰山学者"建设工程专项经费资助项目(编号:ts20110819)

摘　　要：目的:观察脂多糖(LPS)致COPD模型大鼠急性发作时对肝脏的影响。方法:清洁级健康雄性Wistar大鼠24只,随机平均分为正常组,COPD模型组及COPD急性加重组。采用改良熏香烟加气管内注脂多糖的方法建立COPD模型,造模结束后第2天滴加脂多糖建立COPD急性加重模型。6 h后进行肝功能检测,RT-PCR法检测肝肺组织γ-GCS mRNA的表达,观察肺肝病理及超微结构改变。结果:与正常组比较,COPD模型组大鼠碱性磷酸酶(AKP)无统计学意义,谷丙转氨酶(ALT)升高(P<0.05),ALB下降(P<0.05),总结合胆红素(TBIL)明显升高(P<0.01);与正常组比较,COPD急性加重组大鼠白蛋白(ALB)明显下降(P<0.01),ALT、TBIL、AKP均明显升高(P<0.01)。与COPD模型组比较,COPD急性加重组AKP、ALT均升高(P<0.05),ALB下降(P<0.05),TBIL明显升高(P<0.01)。与正常组比较,COPD模型组肺组织中γ-GCS mRNA表达水平显著增高(P<0.01),而肝组织中基因表达水平没有明显变化;COPD急性加重组肝肺组织中γ-GCS mRNA表达水平均显著增高(P<0.01),且与COPD模型组比较有显著差异(P<0.01)。肺肝两脏病理及超微结构均发生了变化。结论:COPD模型大鼠急性加重时可进一步诱导肝脏损害。Objective：Observe whether acute exacerbation of COPD induced by LPS can evoke liver damage. Methods：Divide the rat into three groups randomly：the blank group （A） , the COPD group （B） , and the acute exacerbation of COPD group （C） , 8 rats in each group. Then establish the model of COPD by the improved passive smoking with LPS dropped into the trachea. Based on the model of COPD, drop LPS into the trachea again to establish the acute exacerbation model of the COPD. Six hours later, test the liver function, detect the expression of the γ-GCS mRNA of the hepatopulmonary organization with the method of the RT-PCR, and observe the hepatopulmonary pathology and the change of the uhrastructure. Results： Compared with group A, in group B, the content of ALT is higher（ P 〈 0.05 ）, TBIL significantly increased（ P 〈 0.01 ） ,while ALB drops（ P 〈 0.05 ）, the AKP of the group B had no statistical significance. In group C ,the content of ALT ,TBIL and AKP all rose significantly（ P 〈 0.01 ）, ALB descend obviously. Compared with group B ,the content of ALT and AKP is higher（ P 〈 0.05 ）, TBIL significantly increased （ P 〈 0.01 ）, ALB drops （ P 〈 0.05 ）. Compared with the group A, in the group B, the expression of the γ-GCS gene in lung tissue was significantly increased （P 〈 0.01 ）, which in the liver tissue was not statistically significant in contrast with the normal group;in the group C,the expression of the γ-GCS gene in the liver and lung were obviously higher（ P 〈 0.01 ） ,which has significant difference with the COPD group（ P 〈0.01 ）. The change occurred in the hepatopulmonary pathology and the uhrastructure. Conclusion ： The acute exacerbation of the COPD model rats can further induce the liver damage

关 键 词：慢性阻塞性肺疾病 肝脏损害 COPD模型大鼠 

分 类 号：R259.57[医药卫生—中西医结合]