期刊论文详细信息
Journal of Pharmacological Sciences
Antiproliferative Effect of Echinacoside on Rat Pulmonary Artery Smooth Muscle Cells Under Hypoxia
Yi Zhou2  Ya-Ping Wang1  Feng Tang1  Sheng-Lan Wang1  Xiang-Yun Gai2  Ke-Wu Zeng3  Dian-Xiang Lu1  Ta-Na Wuren1  Jing Ma4  Ri-Li Ge2 
[1] Research Center for High Altitude Medicine, Medical College of Qinghai University, China;Department of Pharmacology, School of Life Science and Biopharmaceutics, Shenyang Pharmaceutical University, China;State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, China;Department of Endemic Diseases, Institute for Endemic Diseases Prevention and Control of Qinghai Province, China
关键词: Tibetan herb;    pulmonary arterial hypertension;    high altitude;    proliferation of rat pulmonary artery smooth muscle cell (PASMC);    apoptosis;   
DOI  :  10.1254/jphs.14072FP
学科分类:药学
来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society
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【 摘 要 】

References(36)Cited-By(1)The main purpose of this study is to evaluate the effect of echinacoside (ECH) on hypoxia-induced proliferation of rat pulmonary artery smooth muscle cells (PASMCs) and the underlying mechanism. PASMCs were incubated under normoxia (nor), hypoxia (hyp), hypoxia + 0.35 mM ECH (hyp + ECH0.35), or hypoxia + 0.4 mM ECH (hyp + ECH0.4) for 24 h. Cell viability was assessed by MTS assays. The morphology of apoptosis was observed by DAPI staining, and apoptosis was quantified by flow cytometric analysis. Caspase-3 activity was determined by immunohistochemistry and real-time PCR, and the expressions of HIF-1α, Bax, Bcl-2, and Fas were determined by real-time PCR. Hypoxia induced significant proliferation of PASMCs, which could be inhibited by ECH in a concentration-dependent manner. This was associated with apoptosis of PASMCs. Z-DEVD-FMK could partly reduce the suppression effect of ECH; protein and gene expression of caspase-3 were significantly higher in the hyp + ECH0.4 and hyp + ECH0.35 groups. ECH significantly increased the expressions of Bax and Fas, but decreased the expressions of Bcl-2 and HIF-1α. ECH could inhibit hypoxia-induced proliferation of rat PASMCs, which is associated with apoptosis of PASMCs and improvement of hypoxia. ECH might be a potential agent for prevention and treatment of hypoxia-induced PAH.

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