摘要
目的:探讨小窝蛋白-1(Caveolin-1)在COPD大鼠肺组织中的表达及其与气道重塑的关系。方法:采用10周龄Wister大鼠20只,随机分为对照组与实验组,每组10只,对照组常规饲养,实验组采用烟熏法+内毒素法建立COPD模型。第91天处死全部大鼠,测定肺功能后取肺组织,采用免疫组织化学法检测Caveolin-1的表达;酶联免疫吸附试验(ELISA)检测各组大鼠肺组织匀浆中白细胞介素-8(IL-8)、肿瘤坏死因子-α(TNF-α)、转化生长因子-β1(TGF-β1)的含量;分析Caveolin-1的表达与IL-8、TNF-α、TGF-β表达的相关性。结果:与对照组比较,实验组大鼠的肺顺应性明显下降,肺弹性阻力及气道阻力显著升高,肺组织TNF-α、IL-8、TGF-β1的含量明显升高,Caveolin-1的表达明显降低,差异均有统计学意义(P<0.05)。大鼠肺组织中Caveolin-1的表达与IL-8、TNF-α、TGF-β1含量呈显著负相关(P<0.05)。结论:Caveolin-1在COPD大鼠肺组织中的表达明显降低,可能通过促进炎性细胞因子的释放与气道重塑参与COPD的发生和发展。
Objective: To investigate the expression of caveolin-1(Caveolin-1) in the lung tissue of rats with COPD and its correla- tion with airway remodeling. Methods: 20 cases of 10 week-old Wister rats were randomly divided into the control group and the experi- mental group, 10 rats in each group. The rats in control group were fed by normal feeding, while the rats in experimental group were fed by the method of smoking and lipopolysaccharide (LPS). All the rats were killed at feeding for 91 days and the lung function were mea- sured. Then immunohistochemical method was used to detect the expression of caveolin-1 in lung tissue, and enzyme-linked immunosor- bent adsorption test (ELISA) was used to detect the interleukin IL-8 (IL-8), tumor necrosis factor alpha (TNF-α and transformation growth factor beta 1 (TGF-β1) in lung tissue. The correlation ofcaveolin-1 expression with IL-8, TNF-α and TGF-β1 expression were analyzed. Results: Compared with the control group, the lung adaptation of rats in experimental group decreased, lung elastic resistance and airway resistance increased, the content of IL-8, TNF-α and TGF-β1 in lung tissue were significantly increased, the expression of caveolin-1 in the lung tissue was significantly decreased (P〈0.05). There was negative correlation of the caveolin-1 expression with IL-8, TNF-α, TGF-β1 contents in the lung tissue. Conclusion: The expression of Caveolin-1 in the lung tissue of rats with COPD was signifi- cantly decreased, Caveolin- 1 might promote the release of inflammatory cytokines and airway remodeling, further participated in the de- velopment of COPD.
出处
《现代生物医学进展》
CAS
2016年第29期5633-5635,5647,共4页
Progress in Modern Biomedicine
基金
黑龙江省卫生厅科研课题(2012-552)