Cooking oil fume-derived PM2.5 induces apoptosis in A549 cells and MAPK/NF-κB/STAT1 pathway activation
Cooking oil fume-derived PM2.5 induces apoptosis in A549 cells and MAPK/NF-κB/STAT1 pathway activation
复制标题
DOI：
10.1007/s11356-018-1262-5
复制
发表时间：
2018-04-01
影响因子：
5.8
通讯作者：
Qi, Cuicui
中科院分区：
文献类型：
--
作者：
Dou, Changming;Zhang, Jie;Qi, Cuicui
烹调油烟是亚洲室内空气污染的主要来源。肺泡细胞是呼吸系统发育的重要参与者，但肺泡细胞是否受到COFs的影响尚不清楚。因此，本研究探讨了COFs对肺泡细胞（A549细胞）的影响，并阐明了COF-PM2.5暴露后肺泡细胞的凋亡机制。COF-PM 2.5处理A549细胞后，细胞活力显著下降，ROS生成增加，LDH和CCK-8水平呈剂量依赖性变化。COF-PM 2.5处理后，上清液中亚硝酸盐浓度增加，SOD活性和GSH循环降低。COF-PM 2.5处理后，考克斯-2、诱导型NO合酶和TNF-α的mRNA水平均升高，且分泌蛋白IL-6和TNF-α的表达也升高。Bax/Bcl-2 mRNA比值增加，caspase-3蛋白被激活。值得注意的是，COF-PM 2.5诱导STAT 1在Tyr 701/Ser 727处的磷酸化以及MAPK通路的NF-κ B B和ERK 1/2、p38和JNK的活化。总之，我们的研究表明，COF-PM 2.5导致A549细胞的炎症、凋亡和细胞损伤，这可能是通过激活MAPK/NF-κ B/STAT 1通路来调节的。
Cooking oil fumes (COFs) are the major sources of indoor air pollution in Asia. It is well known that alveolar cells are key participants in the development of respiratory system; however, it still remains unknown whether alveolar cells are affected by COFs. Therefore, the present study investigated the effects of COFs on alveolar cells (A549 cells) and illuminated its apoptotic mechanism in response to COF-PM2.5 exposure. When A549 cells were exposed to COF-PM2.5, cell viability was substantially decreased, while the generation of ROS increased, and LDH levels and CCK-8 levels gradually changed within a dose-dependent manner. The nitrite concentration in the supernatants was augmented, while the SOD activity and GSH recycling were decreased upon COF-PM2.5. Moreover, COF-PM2.5 treatment increased mRNA levels of COX-2, inducible NO synthase, and TNF-alpha, and Elisa assay suggested that secretory proteins IL-6 and TNF-alpha were also increased. Furthermore, the Bax/Bcl-2 mRNA ratio was increased, and cleaved caspase-3 protein was activated in the A549 cells. Strikingly, COF-PM2.5 induced the phosphorylation of STAT1 at Tyr701/Ser727 and activation of NF-kappa B and ERK1/2, p38, and JNK of the MAPK pathway. In short, our study suggested that COF-PM2.5 resulted in inflammation, apoptosis, and cell damage in A549 cells, which might be modulated via the activation of MAPK/NF-kappa B/STAT1 pathway.