阿托伐他汀在C57BL/6小鼠肺纤维化ROCKⅡ信号通路中的作用  

Atorvastatin in ROCKⅡ signaling pathway of pulmonary fibrosis in C57BL/6 mice

作　　者：陈莹莹[1] 周妍[1] 谭明旗[1] 郑海明[1] 姜珊[1] 郑锐[1] 

机构地区：[1]中国医科大学附属盛京医院呼吸内科,沈阳110000

出　　处：《陕西医学杂志》2015年第1期7-11,共5页Shaanxi Medical Journal

摘　　要：目的:探讨阿托伐他汀对小鼠肺纤维化模型的治疗作用及ROCKII信号转导通路在肺间质纤维化发病中的机制。方法:将60只小鼠随机分为正常对照组,肺纤维化模型组(M),阿托伐他汀(5、10、20、40mg)干预组(B+A5、B+A10、B+A20、B+A40)。应用HE染色、免疫组化、Western-Blot方法,检测ROCKII的表达。结果:经阿托伐他汀干预后,形态学:B+A组纤维化较M组减轻(P<0.01)。免疫组化:B+A组的ROCKⅡ蛋白表达较M组减少(P<0.01);Western-Blot:B+A组ROCKⅡ蛋白表达量减少(P<0.01)。结论:阿托伐他汀可减轻小鼠肺纤维化ROCKII信号通路的通路表达。Objective：To determine the treatment of lung tissues of C57BL/6mice with pulmonary fibrosis（PF）induced by bleomycin at various periods and the effects of ROCKII signal transduction pathway on pulmonary fibrosis.Methods：All 60 mice were randomly divided into 6groups,of which there were model groups of pulmonary fibrosis,atorvastatin groups（5mg、10mg、20mg、40mg）,the other group was control group.we performed histological findings,chemotaxis assays and Western-blot,to detect the expression of RockII.Results：After treatment with atorvastatin,Morphology：B＋A groups of fibrosis than the same period significantly reduced the M group（P〈 0.01）.Immunohistochemistry：Compare with Control group,the expression of ROCKII were markedly inceased,but B＋A group were also significant rueduced（P〈 0.01）;Western blot：The protein expression of ROCK-II markedly decreased in B＋A groups（P〈 0.01）.Conclusion：Atorvastatin reduces the effeets of ROCKII signal transduction pathway on experimental pulmonary fibrosis in mice.

关 键 词：肺纤维化/化学诱导 肺纤维化/病理生理学 博来霉素/治疗应用 模型 动物 小鼠 @阿托伐他汀 

分 类 号：R363.2[医药卫生—病理学]