Acute exposure to PM_2.5 triggers lung inflammatory response and apoptosis in rat

Severe haze events, especially with high concentration of fine particulate matter (PM_2.5), are frequent in China, which have gained increasing attention among public. The purpose of our study was explored the toxic effects and potential damage mechanisms about PM_2.5 acute exposure. Here, the diverse dosages of PM_2.5 were used to treat SD rats and human bronchial epithelial cell (BEAS-2B) for 24 h, and then the bioassays were performed at the end of exposure. The results show that acute exposure to diverse dosages of PM_2.5 could trigger the inflammatory response and apoptosis. The severely oxidative stress may contribute to the apoptosis. Also, the activation of Nrf2-ARE pathway was an important compensatory process of antioxidant damage during the early stage of acute exposure to PM_2.5. Furthermore, the HO-1 was suppression by siRNA that promoted cell apoptosis triggered by PM_2.5. In other words, enhancing the expression of HO-1 may mitigate the cell apoptosis caused by acute exposure to PM_2.5. In summary, our findings present the first time that prevent or mitigate the damage triggered by PM_2.5 through antioxidant approaches was a promising strategy.