GLP-1R过表达对COPD患者气道平滑肌细胞增殖和迁移的影响  

Effects of GLP-1R overexpression on proliferation and migration of airway smooth muscle cells in patients with COPD

作　　者：燕海英[1] 钟甜[1] 刘行仁[1] 杨雁[1] 杨阳[1] 

机构地区：[1]四川省人民医院呼吸科,成都610072

出　　处：《广西医科大学学报》2017年第9期1320-1324,共5页Journal of Guangxi Medical University

摘　　要：目的:探讨胰高血糖素样肽-1受体(GLP-1R)过表达对慢性阻塞性肺病(COPD)患者气道平滑肌细胞(ASMCs)增殖及迁移的影响。方法 :分离培养来自15例COPD患者(观察组)和6例无COPD病史肺部良性肿瘤患者(对照组)的ASMCs。利用Pc DNA3.1(空载体组)和Pc DNA3.1-GLP-1R(过表达组)质粒转染ASMCs,同时设置空白对照组。分别采用q PCR和western blotting法检测GLP-1R表达水平,MTT法和Transwell实验检测ASMCs增殖和迁移能力,酶联免疫吸附试验(ELISA)法检测粒细胞-巨噬细胞集落刺激因子(GM-CSF)、肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-6、IL-8水平。结果:观察组GLP-1R m RNA和蛋白表达水平明显低于对照组(P<0.05),过表达组GLP-1R m RNA及蛋白表达水平明显高于空载体组及空白对照组(P<0.05)。过表达组ASMCs增殖和迁移能力明显低于空载体组、空白对照组(P<0.05),GM-CSF、TNF-α、IL-6、IL-8水平明显亦低于空载体组和空白对照组(P<0.05)。空载体组与空白对照组上述各指标比较,差异均无统计学意义(均P>0.05)。结论:GLP-1R过表达可明显抑制COPD气道平滑肌细胞增殖、迁移,抑制促炎因子释放。Objective： To investigate the effects of GLP-1R overexpression on proliferation and migration of airway smooth muscle cells （ASMCs）in patients with COPD. Methods： ASMCs were collected from 15 pa- tients with COPD （observation group）and 6 patients with benign lung cancer without COPD （control group）. The ASMCs were transfected with PcDNA3. 1 and PcDNA3. 1-GLP-1R plasmids, and blank control group was set at the same time. The expression levels of GLP-1R were detected by qPCR and western blotting, respectively. The proliferation of ASMCs was detected by MTT assay. The migration ability of cells was detected by trans-well assay. The levels of granulocyte macrophage-colony stimulating factor （GM-CSF）, tumor necro- sis factor （TNF）-α, interleukin （IL）-6 and IL-8 were detected by enzyme-linked immuno sorbent assay （ELI- SA）. Results： The expressions of GLP-1R mRNA and protein in the observation group was significantly lower than that in the control group （P〈 0. 05 ）. The GLP-1R mRNA and protein levels were significantly increased in overexpression group, compared with the empty vector group and blank control group （P〈 0. 05 ）. The prolifera- tion and migration abilities of ASMCs in overexpression group were significantly lower than those in empty vec- tor group and blank control group （P〈0. 05）. The levels of GM-CSF, TNF-α, IL-6 and IL-8 in overexpression group were significantly lower than those in empty vector group and blank control group（P〈0.05）. There were no significant differences in above indexes between the empty vector group and the blank control group （P〉0.05）. Conclusion： Overexpression of GLP-1R could significantly inhibit the proliferation and migration of ASMCs in COPD patients, and suppress the release of proinflammatory cytokines.

关 键 词：慢性阻塞性肺病 胰高血糖素样肽-1受体 气道平滑肌细胞 细胞增殖 迁移 

分 类 号：R725.6[医药卫生—儿科]