PM_(2.5)诱导人支气管上皮细胞线粒体损伤

PM_(2.5) induced mitochondrial injury of Human Bronchial Epithelial Cells

流行病学和实验研究表明,PM_(2.5)会对呼吸系统造成损害,但毒性机制还有待深入探讨.本研究采集太原市冬季PM_(2.5),考察其对人支气管上皮细胞(BEAS-2B细胞)的线粒体损伤效应.结果表明,PM_(2.5)会造成细胞线粒体结构变化和功能异常,主要表现为三磷酸腺苷(ATP)水平和线粒体膜电位(MMP)随着PM_(2.5)浓度升高而下降.此外,线粒体功能相关因子PGC-1α、NRF-1和TFAM的蛋白表达量也随着PM_(2.5)浓度的升高呈下降趋势,并在30μg·mL^(-1)时达到最小值.这些结果提示,PM_(2.5)可以导致BEAS-2B细胞发生线粒体结构和功能性变化,进而诱发呼吸系统损伤.

A large number of epidemiological and experimental studies have shown that PM2.5 could induce adverse effects on the respiratory system,but the toxicity mechanism remains to be unclear.Therefore,human bronchial epithelial cells（ BEAS-2 B cells） were exposed to the winter PM2.5 of Taiyuan. The results showed that PM2.5 exposure induced abnormal changes on mitochondria structure and function, such as decreased levels of adenosine triphosphate（ ATP） content and the mitochondrial membrane potential（ MMP） of the cells with the increase of PM2.5 concentration. In addition,the protein expression of PGC-1α,NRF-1 and TFAM was also decreased,and reached the minimum when PM2.5 concentration was 30 μg·mL-1. These results suggested that PM2.5 could induce structural and functional changes of mitochondria in BEAS-2 B cells,which could lead to respiratory injury.