姜黄素激活Nrf2及PPARγ抑制PM2.5所致肺损伤

PM2.5 are severe harmful to human health. PM2.5 can cause cell and tissue damage by oxidative stress and inflammatory, and probably inhibit the synthesis of pulmonary surfactant (PS). So macrophage phagocytic clearance capacity be reduced and the toxic damage of PM2.5 be enhanced. Curcumin can activate the passway of Nrf2 and PPARγ, thus enhance the expression of antioxidant enzymes, inhibit the production of inflammatory cytokines, and may promote pulmonary surfactant synthesis by PPARγ. So Curcumin may reduce PM2.5-induced lung injury. This study will observe PM2.5 on the level of cellular oxidative stress, the expression of inflammatory cytokines, PS synthesis and macrophage phagocytosis, and the effect of the intervention after joined PS, to further explore the mechanism of PM2.5 lung injury. By comparing curcumin, Nrf2 agonists, PPARγ agonists, after PM2.5 exposure, it will be observed that oxidative stress, inflammation levels, PS synthesis of cells and mouse lung tissue and macrophage phagocytosis, in order to explore curcumin and Nrf2 , PPARγ pathway in the defense of the role of of PM2.5 lung injury. This study hopes to provide effective protection for the health of populations in high PM2.5 exposure.

PM2.5对人体健康危害巨大。PM2.5主要通过氧化应激及炎症反应导致细胞和组织损伤，并可能通过抑制肺表面活性物质（PS）的合成，降低巨噬细胞对PM2.5的吞噬清除能力，加重毒性损害。姜黄素能够激活Nrf2和PPARγ，进而增强多种抗氧化酶的表达，抑制炎症因子的产生，并可能通过PPARγ促进肺表面活性物质合成，有助于降低PM2.5所致的肺损伤。本研究拟通过观察PM2.5对细胞氧化应激水平、炎症因子表达、PS合成及巨噬细胞吞噬功能的影响，并观察加入PS的干预效果，进一步探讨PM2.5肺损伤的机制。通过比较姜黄素、Nrf2激动剂、PPARγ激动剂干预后，PM2.5对细胞及小鼠肺组织氧化应激水平、炎症水平，PS合成及巨噬细胞吞噬功能的影响，进一步探讨姜黄素及Nrf2、PPARγ途径在防御PM2.5肺损伤的作用。本研究希望为高PM2.5暴露下的人群健康提供行之有效的保护方法。