内质网应激（ERS）诱导支气管上皮细胞凋亡在慢性阻塞性肺疾病（COPD）的发病中起着重要作用。硫化氢（H2S）是一种新型的气体信号分子，具有抑制凋亡的作用。我们发现，预先给予H2S的供体NaHS可以显著抑制香烟烟雾提取物（CSE）诱导的支气管上皮细胞凋亡，并下调ERS标志性分子CHOP、caspase-4的表达，同时SIRT1/ORP150通路蛋白的表达显著升高。因此，我们推测H2S可以抑制气道上皮细胞发生ERS诱导性凋亡，且可能通过激活SIRT1/ORP150通路来实现，从而延缓COPD的发展。本项目在前期研究的基础上，通过调节H2S的水平，利用细胞转染、Real-time PCR、Western blot、TUNEL等实验技术，从动物以及细胞水平来研究H2S调控ERS在COPD气道上皮细胞凋亡中的作用及其机制，为COPD的防治提供新的靶点和理论基础。

The apoptosis of bronchial epithelial cells induced by endoplasmic reticulum stress (ERS) plays an important role in the pathogenesis of COPD. Hydrogen sulfide (H2S) is a gaseous signal molecule and can inhibit apoptosis. Our previous study found that pretreatment with NaHS, a donor of H2S, could significantly reduce the apoptosis and expressions of ERS maker CHOP and caspase-4 in bronchial epithelial cells induced by cigarette smoke extract (CSE), while the expressions of SIRT1 and ORP150 were significantly increased. Therefore, we hypothesized that H2S could attenuate ERS induced apoptosis in bronchial epithelial cells via SIRT1/ORP150 signaling pathway, which contributed to prevent the progression of COPD. In this study, we will use Real-time PCR, Western-blot, TUNEL test technology to study the protection of H2S on endoplasmic reticulum stress induced apoptosis of bronchial epithelial cells in COPD and the mechanisms, which will provide a new target and theoretical basis for the prevention of COPD.