TY - JOUR AU - Pu, Xian-Juan AU - Li, Jin AU - Zhou, Qiu-Lian AU - Pan, Wen AU - Li, Yong-Qin AU - Zhang, Yuhui AU - Wang, Jinhua AU - Jiao, Zheng PY - 2018 TI - Rosiglitazone inhibits PM2.5-induced cytotoxicity in human lung epithelial A549 cells JF - Annals of Translational Medicine; Vol 6, No 8 (April 26, 2018): Annals of Translational Medicine (Focus on “Breakthroughs in the Treatment of Advanced Lung Cancer: Making Progress Through Innovation”) Y2 - 2018 KW - N2 - Background: Exposure to fine particulate matter Methods: Human lung alveolar epithelial A549 cells were exposed to PM2.5 with or without rosiglitazone (an agonist of PPARγ) treatment. Cellular apoptosis and intracellular oxidative stress were determined by flow cytometry based on FITC Annexin V and DCFH-DA fluorescence, respectively. Western blot was conducted to determine the expression of Bax, Bcl2, PPARγ, P-ERK1/2, ERK1/2, P-STAT3, and STAT3. Results: PPARγ was downregulated in PM2.5-treated A549 cells, and application of rosiglitazone reduced PM2.5-mediated ROS generation and cell apoptosis. In addition, our results indicated that rosiglitazone treatment suppressed PM2.5-induced ERK1/2 and STAT3 activation. Conclusions: Collectively, these data suggested that rosiglitazone protects against PM2.5-induced ROS production and cell apoptosis and represses activation of ERK1/2 and STAT3 signaling in A549 cells. Our results indicated that rosiglitazone is a potential therapeutic agent for PM2.5-induced lung diseases. UR - https://atm.amegroups.org/article/view/19190