腺苷与肺动脉高压的关系一直受到高度关注。有报道腺苷通过A2a受体抑制肺动脉高压形成。本课题组近期发现A2aR基因敲除小鼠出现肺动脉平滑肌、成纤维细胞显著增殖，胶原沉积；低氧下，更为明显。但机制尚不清楚。据报道，激活A2a受体可抑制炎症表达，而炎症与肺动脉高压形成密切相关，有研究认为在炎症反应中起重要作用的基质细胞衍生因子-1（SDF-1，受体为CXCR4）与肺动脉高压形成有关。另有报道激活A2aR可抑制CXCR功能。基于上述发现，本项目拟在整体、细胞和分子水平系统研究SDF-1/CXCR4轴在A2aR基因敲除小鼠肺动脉高压形成中的作用，以探明其作用机制。另有报道，黄芩苷可抑制SDF-1/CXCR4；能预防内毒素休克所致肺动脉高压；可能影响A2aR功能。因此，本项目拟系统研究黄芩苷对低氧性肺动脉高压、SDF-1/CXCR4、A2aR的影响，以期找到一种疗效好而副作用小的治疗肺动脉高压药物。

The relationship between adenosine and pulmonary hypertension is always highly concerned. It has been reported that A2aR could reduce pulmonary hypertension and proliferation of PASMCs induced by hypoxia. Our previous study shows that in chronic hypoxic conditions, proliferation of pulmonary artery smooth muscle cells and collagen deposition in A2aR knockout mice were more significantly than those in wild mice. However, the mechanism is unclear. It is reported that activation of A2aR could inhibit inflammative reaction. As we know, inflammation is closely related to pulmonary hypertension. Stromal cell derived factor -1 (SDF-1) plays an important role in the inflammatory response (CXCR4 is its receptor). Another report is that activating A2aR could inhibit the functions of CXCR. Based on the findings above, this project intends to study the role of SDF-1/CXCR4 axis in pulmonary hypertension induced by hypoxia in A2aR knockout mice through in vitro and in vivo study. It has been reported that baicalin might inhibit SDF-1/CXCR4, prevent pulmonary hypertension induced by endotoxin shock, and affect the function of A2aR. Therefore, the project intends to make sure the effects of baicalin on hypoxic pulmonary hypertension and its mechanism, expecting to find a drug with good efficacy and little side effect to treat pulmonary hypertension.