大气污染中的主要氧化剂臭氧（O3）可诱发或加重哮喘，但其分子机制尚未完全阐明。既往研究显示，经典瞬时受体电位通道6（TRPC6）与卵白蛋白致哮喘气道炎症密切相关。本课题前期在小额探索项目的资助下，发现O3致气道炎症时，小鼠肺组织内硫化氢（H2S）水平降低， TRPC6表达上调；O3攻击TRPC6转基因小鼠后气道炎症反应加重。外源性H2S 可减轻O3引起的损伤。故推测TRPC6在O3致气道炎症反应中起重要作用，内源性H2S可能起保护作用。因此，本课题在前期工作基础上，拟用TRPC6转基因和基因敲除小鼠及气道上皮细胞作为研究对象，结合分子生物学和膜片钳等技术，进一步探讨TRPC6及其上下游信号分子在O3致气道炎症中的作用以及H2S可能作用的靶点。该研究将有助于阐明O3致哮喘的分子机制，并为应用H2S防治哮喘提供新的理论依据，对大气污染环境下敏感人群的健康保护及指导临床治疗有重要意义。

Ozone (O3), a major oxidant in atmospheric pollutants, usually triggers or aggravates asthma. However, the detailed molecular mechanism has not been fully elucidated. Our previous research has shown that OVA-induced airway inflammation is closely associated with classical transient receptor potential channel 6 (TRPC6). In addition, we have conducted experiments funded by a small project and found that the content of hydrogen sulfide (H2S) was reduced, the expression of TRPC6 was upregulated in the lung tissue of wide-type (WT) mice exposed to O3. Furthermore, comparing with WT mice, exposure of TRPC transgenic mice to O3 induced more severe injury and O3-induced injuries were attenuated by administration of H2S in WT mice. We therefore speculate that TRPC6 plays a very important role in O3-induced airway inflammation, which can be mitigated by H2S. Based on our study above, TRPC6 transgenic and knockout mice, airway epithelial cells, molecular biology and patch-clamp techniques are used to investigate the roles of TRPC6 and its signaling pathway in O3-induced airway inflammation and the possible targets of H2S therapy. The study will elucidate the molecular mechanisms of O3-induced asthma and provide a new theoretical basis for the H2S prevention. These are significant for the health care of people sensitive to atmospheric pollutants and may provide guidance for clinical treatment of atmospheric pollutants-induced asthma.