陕西医学杂志
陝西醫學雜誌
협서의학잡지
SHAANXI MEDICAL JOURNAL
2015年
1期
7-11
,共5页
陈莹莹%周妍%谭明旗%郑海明%姜珊%郑锐
陳瑩瑩%週妍%譚明旂%鄭海明%薑珊%鄭銳
진형형%주연%담명기%정해명%강산%정예
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
肺纖維化/化學誘導%肺纖維化/病理生理學%博來黴素/治療應用%模型, 動物%小鼠%阿託伐他汀
폐섬유화/화학유도%폐섬유화/병리생이학%박래매소/치료응용%모형, 동물%소서%아탁벌타정
Pulmonary fibrosis/chemically induced%Pulmonary fibrosis/physiopathology%Bleomycin/therapeuticuse%Models,animal%Mice%Atorvastatin
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 ROCK Ⅱ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。
目的:探討阿託伐他汀對小鼠肺纖維化模型的治療作用及ROCKII信號轉導通路在肺間質纖維化髮病中的機製。方法:將60隻小鼠隨機分為正常對照組,肺纖維化模型組(M ),阿託伐他汀(5、10、20、40mg )榦預組(B+ A5、B+ A10、B+ A20、B+ A40)。應用 HE染色、免疫組化、Western‐Blot方法,檢測ROCKII的錶達。結果:經阿託伐他汀榦預後,形態學:B+ A組纖維化較M 組減輕(P <0.01)。免疫組化:B+A組的ROCKⅡ蛋白錶達較M 組減少(P <0.01);Western‐Blot :B+ A 組 ROCK Ⅱ蛋白錶達量減少(P<0.01)。結論:阿託伐他汀可減輕小鼠肺纖維化ROCKII信號通路的通路錶達。
목적:탐토아탁벌타정대소서폐섬유화모형적치료작용급ROCKII신호전도통로재폐간질섬유화발병중적궤제。방법:장60지소서수궤분위정상대조조,폐섬유화모형조(M ),아탁벌타정(5、10、20、40mg )간예조(B+ A5、B+ A10、B+ A20、B+ A40)。응용 HE염색、면역조화、Western‐Blot방법,검측ROCKII적표체。결과:경아탁벌타정간예후,형태학:B+ A조섬유화교M 조감경(P <0.01)。면역조화:B+A조적ROCKⅡ단백표체교M 조감소(P <0.01);Western‐Blot :B+ A 조 ROCK Ⅱ단백표체량감소(P<0.01)。결론:아탁벌타정가감경소서폐섬유화ROCKII신호통로적통로표체。
Objective:To determine the treatment of lung tissues of C57BL/6 mice with pulmonary fibro‐sis(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 6 groups ,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 .