山东医药2016，Vol.56Issue(45)：15-18,4.DOI:10.3969/j.issn.1002-266X.2016.45.005
慢性阻塞性肺疾病大鼠肺组织JNK／SAPK 水平变化及意义
Changes in Ievels of JNK/SAPK of rats with chronic obstructive pulmonary disease
摘要
Abstract
Objective To investigate the changes in levels of c-Jun N-terminal kinase /stress-activated protein kinase (JNK/SAPK)in the lung tissues of rats with chronic obstructive pulmonary disease (COPD).Methods Sixteen Ⅱ male Wistar rats were randomly divided into two groups:the control group and COPD group.The control group was not treated, while the COPD group was stimulated with smoke to set up COPD models.After models were established,we detected the lung pathology through optical microscope,pulmonary function through animal pulmonary instrument,TNF-αexpression in lung tissue through ELISA,JNK/SAPK expression through immunohistochemistry,and JNK mRNA expression through RT-PCR.Results In the COPD group,light microscope showed that there was a large number of inflammatory cell infiltra-tion,alveolar fusion,and alveolar reduction,which proved the COPD model was successful.Compared with the control group,FEV0.3 /FVC decreased,Ri and Re increased,and Cldyn decreased (P <0.05 or P <0.01 ),and TNF-αin-creased in the COPD group (P <0.05).Immunohistochemistry showed that JNK/SAPK expression improved in the COPD group.RT-PCR result showed JNK mRNA expression increased in the COPD group as compared with that of the control group (all P <0.05).JNK mRNA expression was positively correlated with TNF-α(r =0.751,P <0.05).Conclusion The level of JNK/SAPK increases in smoke-stimulated COPD rats,which can cause airway inflammation and emphysema, and promote the occurrence of COPD through activating smoke-induced inflammatory cytokines.关键词
慢性阻塞性肺疾病/C-Jun 氨基末端蛋白激酶/应激激活蛋白激酶/作用机制Key words
chronic obstructive pulmonary disease/c-Jun N-terminal kinase/stress-activated protein kinase/effect mechanism分类
医药卫生引用本文复制引用
田雪,张杏怡,李锋,肖辉,周新..慢性阻塞性肺疾病大鼠肺组织JNK／SAPK 水平变化及意义[J].山东医药,2016,56(45):15-18,4.基金项目
国家自然科学基金面上项目（81470218）；中国医师协会呼吸免疫专项课题（2014）。 （）
