微囊蛋白1抗体对汽油机尾气致大鼠肺损伤的作用
Alleviation Effect of Caveolin-1 Antibody on Pulmonary Injury in Rats Caused by Exposure to Gasoline Engine Exhaust
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摘要:
目的 观察微囊蛋白1(caveolin-1)抗体对汽油机尾气所致肺损伤的保护作用。 方法 雄性健康SD大鼠42只,随机分为正常对照组6只、染毒对照组6只、干预组30只(分1、2、4、8、12周亚组,每亚组6只)。正常对照组不作任何处理,正常喂饲;染毒对照组以汽油机尾气持续染毒12周,每天染毒2 h;干预组各亚组在开始染毒后的前2周让实验动物吸入超声雾化的caveolin-1多克隆抗体,并分别用汽油机尾气染毒1、2、4、8、12周。各组大鼠在最后一次染毒24 h后处死,对肺组织进行常规病理形态学观察,用免疫组织化学技术检测肺部caveolin-1和转化生长因子β1(TGF-β1)表达变化。 结果 染毒对照组大鼠体重明显较正常对照组轻,干预组体重介于正常对照组与染毒对照组之间。干预组炎症反应较染毒对照组明显减轻,纤维组织增生减少。正常对照组可以检测到较弱的caveolin-1表达;染毒对照组则几乎检测不到;干预组表达先增强后减低,但实验后期仍较染毒对照组略高。TGF-β1表达在正常对照组最低;染毒对照组最高;干预组逐渐升高,但较染毒对照组明显减弱。 结论 早期使用caveolin-1多克隆抗体可部分减轻汽油机尾气造成的肺部损伤。 Abstract:Objective To observe if there is a protective effect of caveolin-1 antibody on chronic lung injury caused by gasoline engine exhaust in rats. Methods Forty-two health male SD rats were randomly divided into 1 blank control group, 1 model control group, and 5 experimental groups. The blank control group was fed normally without any treatment. The model control group was exposed to gasoline engine exhaust 2 h/d for 12 weeks in a self-made exposure cabinet where the exhaust was discharged into. The experimental animals inhaled ultrasonic atomized caveolin-1 polyclonal antibodies into their lungs and then were exposed to gasoline engine exhaust for 1, 2, 4, 8, and 12 weeks respectively. All the animals were sacrificed 24 h after the last exposure and pathological morphology of their lungs was examined. Expressions of caveolin-1 and transforming growth factor β1 (TGF-β1) in the lung were detected by immunohistochemistry technique. Results The body weight of the experimental groups was significantly decreased after exhaust exposure, but was higher than that of the model control group. The lesions and fibroplasias of the experimental group were significantly reduced compared with the model control group. The expression level of caveolin-1, in comparison with the blank controls, was reduced to a barely detectable level after the animals inhaled the gasoline engine exhaust, while it was first increased, then decreased, and finally reached a level slightly higher than that of the model controls in animals pre-administrated with caveolin-1 polyclonal antibodies. The expression level of TGF-β1 was increased significantly after the rats inhaled gasoline engine exhaust, and was slowly increased in the exposed rats with caveolin-1 polyclonal antibody pre-administration. Conclusion The early use of caveolin-1 antibody can partially mitigate the pulmonary injury in rats caused by gasoline engine exhaust.
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