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学科主题临床医学
Sodium hydrosulfide alleviated pulmonary vascular structural remodeling induced by high pulmonary blood flow in rats
Li, Xiao-hui; Du, Jun-bao; Bu, Ding-fang; Tang, Xiu-ying; Tang, Chao-shu
关键词hydrogen sulfide pulmonary hypertension structure remodeling nitric oxide/nitric oxide synthase carbon monoxide/heme oxygenase
刊名ACTA PHARMACOLOGICA SINICA
2006-08-01
DOI10.1111/j.1745-7254.2006.00353.x
27期:8页:971-980
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Chemistry, Multidisciplinary ; Pharmacology & Pharmacy
研究领域[WOS]Chemistry ; Pharmacology & Pharmacy
关键词[WOS]NITRIC-OXIDE SYNTHASE ; HYDROGEN-SULFIDE ; CARBON-MONOXIDE ; SUBCELLULAR-DISTRIBUTION ; CELL-PROLIFERATION ; ENDOTHELIAL-CELLS ; AORTOCAVAL SHUNT ; GROWTH-FACTOR ; SHEAR-STRESS ; HYPERTENSION
英文摘要

Aim: To explore the possible role of endogenous hydrogen sulfide (H2S), a novel gasotransmitter, in the pathogenesis of pulmonary vascular structural remodeling (PVSR) induced by high pulmonary blood flow.

Methods: Thirty-two Sprague-Dawley male rats were randomly divided into sham, shunt, sham+NaHS (a H2S donor) and shunt+NaHS groups. Rats in shunt and shunt+NaHS groups underwent an abdominal aorta-inferior vena cava shunt, and rats in shunt+NaHS and sham+NaHS groups were intraperitoneally injected with NaHS. PVSR was investigated using optical microscope and transmission electron microscope. Lung tissue H2S was evaluated by sulfide-sensitive electrodes. Nitric oxide synthase (NOS), heme oxygenase (HO-1), proliferative cell nuclear antigen (PCNA) and extracellular signal-regulated kinase (ERK) activation were analyzed by Western blotting.

Results: After 11 weeks of shunting, PVSR developed with a decrease in lung tissue H2S production and an increase in nitric oxide (NO). However, lung tissue carbon monoxide (CO) did not change. After the treatment with NaHS for 11 weeks, H2S donor ameliorated PVSR and downregulated PCNA expression and ERK activation with an increase in lung tissue CO production and HO-1 protein expression but a decrease in NO production, NOS activity and eNOS protein expression in shunted rats.

Conclusions: H2S exerted a regulatory effect on PVSR induced by high pulmonary blood flow. Meanwhile, H2S down-regulated the ERK/MAPK signal pathway, inhibited the NO/NOS pathway and enhanced the CO/HO pathway in rats with high pulmonary blood flow.

语种英语
WOS记录号WOS:000239306600003
Citation statistics
Cited Times:22[WOS]   [WOS Record]     [Related Records in WOS]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/66060
Collection北京大学第一临床医学院_儿科
作者单位1.Peking Univ, Dept Pediat, Hosp 1, Key Lab Mol Cardiovasc Dis,Minist Educ, Beijing 100034, Peoples R China
2.Peking Univ, Lab Ctr, Hosp 1, Beijing 100034, Peoples R China
3.Peking Univ, Electron Microscopy Lab, Hosp 1, Beijing 100034, Peoples R China
4.Peking Univ, Hlth Sci Ctr, Dept Physiol, Beijing 100083, Peoples R China
Recommended Citation
GB/T 7714
Li, Xiao-hui,Du, Jun-bao,Bu, Ding-fang,et al. Sodium hydrosulfide alleviated pulmonary vascular structural remodeling induced by high pulmonary blood flow in rats[J]. ACTA PHARMACOLOGICA SINICA,2006,27(8):971-980.
APA Li, Xiao-hui,Du, Jun-bao,Bu, Ding-fang,Tang, Xiu-ying,&Tang, Chao-shu.(2006).Sodium hydrosulfide alleviated pulmonary vascular structural remodeling induced by high pulmonary blood flow in rats.ACTA PHARMACOLOGICA SINICA,27(8),971-980.
MLA Li, Xiao-hui,et al."Sodium hydrosulfide alleviated pulmonary vascular structural remodeling induced by high pulmonary blood flow in rats".ACTA PHARMACOLOGICA SINICA 27.8(2006):971-980.
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