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目的探讨Caveolin-1与TGF-β1在汽油机尾气致慢性肺损伤中的表达规律。方法雄性健康SD大鼠54只,随机分为为正常对照组6只,实验组48只(实验组又分1 d、3 d、5 d、7 d、2 w、4 w、8 w和12 w亚组,每亚组6只);将实验各组动物置于自制的染毒箱后启动汽油机,将汽油机尾气通入染毒箱进行染毒,每天染毒2h;各实验组分别染毒1 d、3 d、5 d、7 d、2周、4周、8周、12周,实验各组的动物在最后一次染毒24 h后被处死,用免疫组织化学技术检测肺部Caveolin-1与TGF-β1表达变化;用图像分析技术对免疫组化结果进行分析。结果 Caveolin-1在正常对照组支气管上皮、肺泡上皮、成纤维细胞呈较强的阳性表达,主要位于细胞膜上;汽油机尾气染毒后,Caveolin-1表达先增强后减弱,在7 d后达高峰,此后逐渐降低,2周后显著降低,此后一直维持在很低的水平表达。TGF-β1主要表达于支气管上皮、肺泡上皮、成纤维细胞胞浆;在正常对照组表达微弱,1 d、3 d组的表达强度较对照组略高,5 d后表达逐渐增强,至2周时达高峰,此后稍有降低,但仍然较正常对照组高。结论 Caveolin-1与TGF-β1均参与了汽油机尾气造成的肺慢性损伤的病理生理过程,且其表达时相大致相反,提示Caveolin-1对TGF-β1有抑制作用。
Objective To investigate the expression of Caveolin-1 and TGF-β1 in chronic lung injury induced by tail gas in gasoline engine. Methods Fifty-four male Sprague-Dawley rats were randomly divided into six groups: normal control group (n = 48) and experimental group (n = 48). The experimental group was divided into 1 d, 3 d, 5 d, 7 d, 2 w, 4 w, w subgroups, 6 in each subgroup). The experimental animals in each group were placed in a homemade poisoning box and then the gasoline engine was started. The tail gas of the gasoline engine was exposed to the poisoning box for exposure for 2 hours. The experimental groups were exposed to 1 d, 3 d, 5 d, 7 d, 2weeks, 4weeks, 8weeks and 12weeks. Animals in each experimental group were sacrificed 24 h after the last exposure, and immunohistochemistry was used to detect the expression of Caveolin- 1 and TGF-β1 expression; image analysis of immunohistochemistry results were analyzed. Results Caveolin-1 showed strong positive expression in bronchial epithelium, alveolar epithelium and fibroblasts in normal control group, mainly located on the cell membrane. Caveolin-1 expression increased first and then decreased and reached the peak at 7 d after gasoline engine exhaust , Then gradually decreased after 2 weeks significantly reduced, since then has been maintained at a very low level of expression. The expression of TGF-β1 was mainly in the bronchial epithelium, alveolar epithelium and fibroblast cytoplasm. The expression of TGF-β1 was weak in the normal control group. The expression intensity of TGF-β1 was slightly higher than that of the control group on day 1 and 3, Peak, then slightly lower, but still higher than the normal control group. Conclusions Both Caveolin-1 and TGF-β1 are involved in the pathophysiological process of chronic lung injury induced by gasoline engine exhaust, and their expression phases are roughly opposite, suggesting that Caveolin-1 inhibits TGF-β1.