肺纤维化发病机制不明，无有效防治措施，是严重威胁人类健康的疾病。Ras相关蛋白（Rab6）具有调节细胞的生长、分化和蛋白质运输的作用而备受关注。我们前期研究表明持续的大气细颗粒物（PM2.5）刺激能够诱导肺纤维化的产生，抑制肺泡干细胞再生能力，Rab6在肺纤维化样本中高表达，Notch低表达，Rab6能够抑制肺细胞干性。我们提出“Rab6通过Notch通路抑制肺泡干细胞再生能力，促进PM2.5诱导肺纤维化发生”这一新的分子机制。本项目拟通过免疫共沉淀等实验阐明Rab6抑制Notch通路的分子机制和对肺泡干细胞再生能力的影响，并通过Rab6过表达小鼠肺纤维化模型探讨动物抑制Rab6是否能缓解肺纤维化的各项指标，阐明其作为肺纤维化治疗分子靶标的可能性。以上机制的阐明，将为肺纤维化的靶点治疗提供新的依据。

The pathogenesis of pulmonary fibrosis is unknown, and there are no effective prevention measures. It is a serious threat to human health. The Ras-associated protein (Rab6) is attracting attention for its role in regulating cell growth, differentiation, and protein trafficking. Our previous studies showed that persistent atmospheric fine particles (PM2.5) stimulation can induce the generation of pulmonary fibrosis and inhibit the regeneration of alveolar stem cells. Rab6 is highly expressed in lung fibrosis samples, and Notch is lowly expressed. Rab6 can inhibit the dryness of lung cells. We proposed that "Rab6 inhibits the regeneration of alveolar stem cells through the Notch pathway and promotes PM2.5-induced pulmonary fibrosis" as a new molecular mechanism. This project intends to elucidate the molecular mechanisms underlying Rab6's inhibition of Notch pathway and its effect on alveolar stem cell regeneration through experiments such as co-immunoprecipitation, and to determine whether Rab6 can inhibit pulmonary fibrosis in animals by Rab6 over-expressing mouse lung fibrosis model. Indicators to elucidate its potential as a molecular target for the treatment of pulmonary fibrosis. The elucidation of the above mechanisms will provide a new basis for target treatment of pulmonary fibrosis.