WANG Ye , CHENG Wei-bo , XU Yun-yi , HE Xiao-li , HUANG Qin , LUO Jian . Alleviation Effect of Caveolin-1 Antibody on Pulmonary Injury in Rats Caused by Exposure to Gasoline Engine Exhaust[J]. Journal of Environmental and Occupational Medicine, 2013, 30(1): 15-20.
Citation: WANG Ye , CHENG Wei-bo , XU Yun-yi , HE Xiao-li , HUANG Qin , LUO Jian . Alleviation Effect of Caveolin-1 Antibody on Pulmonary Injury in Rats Caused by Exposure to Gasoline Engine Exhaust[J]. Journal of Environmental and Occupational Medicine, 2013, 30(1): 15-20.

Alleviation Effect of Caveolin-1 Antibody on Pulmonary Injury in Rats Caused by Exposure to Gasoline Engine Exhaust

  • 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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