Hydrogen sulfide induces apoptosis of pulmonary artery smooth muscle cell in rats with pulmonary hypertension induced by high pulmonary blood flow
Hydrogen sulfide induces apoptosis of pulmonary artery smooth muscle cell in rats with pulmonary hypertension induced by high pulmonary blood flow
复制标题
硫化氢诱导高肺血流肺动脉高压大鼠肺动脉平滑肌细胞凋亡
DOI：
10.3760/cma.j.issn.0366-6999.2009.24.023
复制
发表时间：
2009-12-20
影响因子：
6.1
通讯作者：
Du Jun-bao
中科院分区：
文献类型：
--
作者：
Li Wei;Jin Hong-fang;Du Jun-bao
Background Abnormal apoptosis of pulmonary artery smooth muscle cells (PASMCs) is an important pathophysiological process in the pulmonary artery structural remodeling and pulmonary hypertension. We investigated possible effect of endogenous hydrogen sulfide (H2S) on apoptosis of PASMCs during the development of pulmonary hypertension induced by high pulmonary blood flow.Methods Thirty-nine male Sprague-Dawley rats were randomly assigned to 4-week control, 4-week shunt, 4-week shunt+propargylglycine (PPG), 11-week control, 11-week shunt and 11-week shunt+sodium hydrosulfide (NaHS) groups. Rats in 4-week shunt, 4-week shunt+PPG, 11-week shunt and 11-week shunt+NaHS groups underwent an abdominal aorta-inferior vena cava shunt. Rats in 4-week shunt+PPG group were intraperitoneally injected with PPG an inhibitor of endogenous H2S production, for 4 weeks. Rats in 11-week shunt+NaHS group were intraperitoneally injected with NaHS, a H2S donor, for 11 weeks. Lung tissue H2S was evaluated by sulfide-sensitive electrode. Apoptosis of PASMCs were detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL). Expressions of Fas, bcl-2 and caspase-3 in the PASMCs were analyzed with immunochemical staining.Results Four weeks after the shunting operation, the apoptosis of PASMCs and expression of Fas and caspase-3 were significantly decreased (P
