近年来，肺血管炎症反应在肺动脉高压发病机制中的意义受到高度关注。本课题在申请者对内源性硫化氢与肺动脉高压的系列研究基础上，以野百合碱诱导肺动脉高压大鼠为研究模型，研究肺动脉高压大鼠肺血管炎症反应形成过程中内源性硫化氢体系的动态变化规律；通过激活或抑制内源性硫化氢体系，观察肺动脉高压大鼠肺血管炎症反应和肺动脉内皮细胞炎症因子合成和释放的改变，揭示内源性硫化氢对肺动脉高压形成中肺动脉内皮细胞炎症反应的调节作用；以核转录因子-κB (NF-κB) 信号通路为切入点，揭示硫化氢抑制肺动脉高压大鼠肺动脉内皮细胞炎症反应的信号转导通路；以NF-κB p65 cys38巯基基团为靶点，探索硫化氢抑制肺动脉内皮细胞NF-κB 信号通路的分子机制。通过上述研究，以期阐明内源性硫化氢对肺动脉高压大鼠肺血管炎症反应的调节作用及分子机制，进一步深化肺动脉高压的炎症机制理论，为探寻肺动脉高压的治疗靶点提供新思路。

Recently, great attention has been paid to the pulmonary vascular inflammatory response in the study of the mechanisms for pulmonary hypertension. Based on the applicant's previous studies on endogenous hydrogen sulfide and pulmonary hypertension, the present study is designed to investigate the changing profile of endogenous hydrogen sulfide pathway in the process of pulmonary vascular inflammatory response in monocrotaline-induced pulmonary hypertensive rats. By activating and inhibiting the endogenous hydrogen sulfide pathway, and examining the changes in pulmonary vascular inflammatory response in pulmonary hypertensive rats as well as the synthesis and secretion of inflammatory factors by pulmonary artery endothelial cells, the study is designed to elucidate the regulatory effect of endogenous hydrogen sulfide on pulmonary vascular inflammatory response in pulmonary hypertension. Furthermore, targeting on NF-κB pathway, the applicant aims to discover the signaling pathway by which hydrogen sulfide inhibits pulmonary vascular inflammatory response in pulmonary hypertension. Meanwhile, focusing on the NF-κB p65 cysteine 38 thiol group, the applicant is to examine the molecular mechanisms by which hydrogen sulfide inhibits pulmonary artery endothelial cell inflammatory response. The findings concerning the regulatory effect of endogenous hydrogen sulfide on the pulmonary vascular inflammatory response in rats with pulmonary hypertension and the mechanisms would greatly deepen the understanding of the inflammatory mechanisms for pulmonary hypertension and provide new research strategy for discovering therapeutic target for pulmonary hypertension.