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The Influence of Mixed Air Pollutants on the Expression of CC16 in Serum and Lung Tissue of Rats

Author: LiKeJun
Tutor: SunYanBo；XiaoChunLing
School: Jilin University
Course: Pathogen Biology
Keywords: Atmospheric mixing pollutants Rats Serum Lung tissue CC16
CLC: R114
Type: Master's thesis
Year: 2011
Downloads: 35
Quote: 0
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Abstract


Purpose urban air pollution problems have been a serious threat to human health, toxicity mechanism of lung injury in order to explore the atmospheric pollutants through the atmosphere to co-pollutants dye dust exposure experiments, knowledge of the atmospheric pollution mixtures role of mouse serum and lung tissue expression levels of CC16, damage the human body to provide a basis for the prevention of air pollution. This study established by experimental rats injected saline suspension and inhalation of SO2, NO2, CO air mixture containing PM2.5 under ether anesthesia, animals stained dust exposure model. Measured by ELISA in serum and BALF of CC16, real-time quantitative RT-PCR analysis lung tissue CC16mRNA, expression, immunohistochemistry method for the determination of the expression of CC16 in the lung tissue. Exposure 1d and 30d rats lung tissue CC16 content was significantly higher than that in the control group, exposed to 7d of the lung tissue CC16 was significantly lower than the control group and exposure 1d group (P lt; 0.01) exposed to 30d lung tissue CC16 expression was significantly higher than the exposure 1d and 7d group (P lt; 0.01); exposure the 7d lung tissue CC16mRNA expression was higher, exposed to 1d group and 30 days (P lt; 0.05); exposed to the 30d of serum CC16 was significantly higher than that in the control group, exposed 1d and 7d group (P lt; 0.05); the BALF in CC16 showed no significant change . Conclusion 1. Atmosphere mixed pollutant early inflammatory response in (d), rat lung tissue CC16 significantly higher than that in the control group, serum and BALF CC16 showed no significant change, there is a cause lung tissue CC16 higher trend in the early inflammatory . 2 exposure 7d, which CC16 in the lung tissue of rats was significantly lower than the control group, the serious injury of lung tissue cells and capillary endothelial cells. And CC16mRNA expression was significantly higher than that in the control group, indicating that the compensatory damage 7d process CC16mRNA enhanced expression, CC16mRNA levels as sensitive biological indicators of early lung injury. 3 exposure 30d, serum CC16 content was significantly increased, indicating that exposure post-alveolar tissue self-healing process and compensatory CC16 increased synthesis of serum CC16 were significantly increased. 4 in lung tissue the CC16 was reduced as an important indicator of early lung injury. Serum CC16 levels increased lung tissue has entered a repair period. Did not change significantly in BALF CC16 CC16 levels in BALF can not as a point of reference to determine the lung tissue damage.

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