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目的探讨FHL1与COPD大鼠肺血管重塑的关系及肺动脉平滑肌细胞增殖及表型转换在其中的作用。方法将20只雄性SD大鼠随机分为正常组及COPD组,每组10只。COPD组香烟烟雾暴露80 d复制COPD模型。图像分析法测定肺小动脉管壁厚度占外径的百分比(WT%)和管壁面积占血管总面积的百分比(WA%)。Western-blot法检测肺组织FHL1蛋白,荧光定量PCR法检测肺组织FHL1 mRNA。免疫组化法检测肺小动脉FHL1、α-actin及vimentin;PCNA法检测肺动脉平滑肌增殖细胞的阳性细胞率(PI);t检验及直线相关进行数据分析。结果 COPD组WT%和WA%较正常组升高(P<0.05),COPD组肺组织FHL1蛋白及mRNA(133.250±25.499和4.963±0.692)较正常组(51.188±18.259和1.697±0.360)升高(P<0.05)。COPD组肺小动脉FHL1、vimentin、α-actin及PI(0.316±0.093、0.085±0.030、0.219±0.049和0.575±0.076)较正常组(0.241±0.093、0.069±0.023、0.163±0.042和0.429±0.092)升高(P<0.05)。肺小动脉FHL1表达与WT%、WA%、vimentin及PI呈正相关(P<0.05),但肺小动脉FHL1表达与α-actin表达无相关性(P>0.05)。结论 COPD大鼠肺血管FHL1增加与肺血管重塑相关,FHL1可能通过增加肺血管平滑肌细胞增殖及促进平滑肌细胞合成表型转换参与COPD肺血管重塑。
Objective To investigate the relationship between FHL1 and pulmonary vascular remodeling in rats with chronic obstructive pulmonary disease (COPD) and the role of pulmonary artery smooth muscle cell proliferation and phenotype transduction. Methods Twenty male SD rats were randomly divided into normal group and COPD group, with 10 rats in each group. The COPD group was exposed to cigarette smoke for 80 days to replicate the COPD model. Image analysis was performed to determine the ratio of the wall thickness of the pulmonary arterioles to the outer diameter (WT%) and the percentage of wall area to the total area of the blood vessels (WA%). FHL1 protein in lung tissue was detected by Western-blot and FHL1 mRNA in lung tissue by fluorescence quantitative PCR. The pulmonary arterioles FHL1, α-actin and vimentin were detected by immunohistochemistry. The positive cell rate (PI) of pulmonary artery smooth muscle cells were detected by PCNA. The t test and linear correlation were used to analyze the data. Results The percentages of WT% and WA% in COPD group were significantly higher than those in normal group (P <0.05). The levels of FHL1 protein and mRNA in COPD group were significantly higher than those in control group (51.288 ± 18.259 and 1.697 ± 0.360) (133.250 ± 25.499 and 4.963 ± 0.692, respectively) (P <0.05). The pulmonary arterioles FHL1, vimentin, α-actin and PI of COPD group (0.316 ± 0.093,0.085 ± 0.030,0.219 ± 0.049 and 0.575 ± 0.076) were significantly higher than those of normal group (0.241 ± 0.093,0.069 ± 0.023,0.163 ± 0.042 and 0.429 ± 0.092) ) Increased (P <0.05). The expression of FHL1 in pulmonary arterioles was positively correlated with WT%, WA%, vimentin and PI (P <0.05). However, there was no correlation between FHL1 expression and α-actin expression in pulmonary arterioles (P> 0.05). Conclusions The increase of FHL1 in pulmonary vessels of COPD rats is associated with remodeling of pulmonary vessels. FHL1 may participate in the pulmonary remodeling of COPD by increasing the proliferation of pulmonary vascular smooth muscle cells and promoting the synthesis phenotype of smooth muscle cells.