Overexpression of Lias Gene Alleviates Pulmonary Injury Induced by fine particulate matter in Mice

Abstract Oxidative stress, inflammation is generally regarded as important toxicity mechanisms induced by fine particulate matter (PM2.5). The antioxidant baselines of human body affect the intensity of oxidative stress in vivo. Our study aimed to evaluate the role of endogenous antioxidant capacity in PM2.5-induced pulmonary injury using a novel mouse model (LiasH/H) which approximately increased 150% endogenous antioxidant capacity relative to its wild-type counterpart. LiasH/H and C57BL/6J mice were randomly divided into control group and PM2.5 exposure group (n = 10) respectively. The PM2.5-exposed group and the control group mice were intratracheally instilled with PM2.5 and saline respectively once daily for 7 consecutive days. The main pulmonary pathological changes, oxidative stress and inflammatory biomarkers levels were examined. The results showed that oxidative stress was significantly increased in all mice after PM2.5 exposure. Overexpression of Lias gene significantly increased the capacity against oxidative stress and decreased inflammatory responses caused by PM2.5 in model mice compared with the control mice. Antioxidant capacity in the LiasH/H mice was elevated through increased NRF2, the activation of ROS-p38MAPK- NRF2 signaling pathway. The novel mouse model is useful for clarifying the mechanisms of pulmonary injury induced by PM2.5.