کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8474353 | 1550423 | 2015 | 14 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Salidroside attenuates chronic hypoxia-induced pulmonary hypertension via adenosine A2a receptor related mitochondria-dependent apoptosis pathway
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کلمات کلیدی
MCAPPAHHUVECSA2ARRVSPMYH11PASMCsCOPD - بیماری مزمن انسدادی ریهChronic obstructive pulmonary disease - بیماری مزمن انسدادی ریهApoptosis - خزان یاختهایSalidroside - سالیدروزیدHuman umbilical vein endothelial cells - سلول های اندوتلیالی ورید ناف انسانPulmonary arterial smooth muscle cells - سلول های عضلانی صاف شریانی ریویPulmonary arterial hypertension - فشار خون شریانی ریویright ventricular systolic pressure - فشار سیستولیک بطن راستChronic hypoxia - هیپوکسی مزمنAdenosine A2A receptor - گیرنده آدنوزین A2A
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Pulmonary arterial hypertension (PAH) is characterized by pulmonary arterial remodeling mainly due to excess cellular proliferation and apoptosis resistance of pulmonary arterial smooth muscle cells (PASMCs). Salidroside, an active ingredient isolated from Rhodiola rosea is proposed to exert protective effects against PAH. However, the function of salidroside in PAH has not been investigated systematically and the underlying mechanisms are not clear. To investigate the effects of salidroside on PAH, the mice in chronic hypoxia model of PAH were given by an increasing concentration of salidroside (0, 16Â mg/kg, 32Â mg/kg, and 64Â mg/kg). After salidroside treatment, the chronic hypoxia-induced right ventricular hypertrophy and pulmonary arterial remodeling were attenuated, suggesting a protective role played by salidroside in PAH. To explore the potential mechanisms, the apoptosis of PASMCs after salidroside treatment under hypoxia conditions were determined in vivo and in vitro, and also the mitochondria-dependent apoptosis factors, Bax, Bcl-2, cytochrome C, and caspase 9 were examined. The results revealed that salidroside reversed hypoxia-induced cell apoptosis resistance at least partially via a mitochondria-dependent pathway. In addition, salidroside upregulated the expression of adenosine A2a receptor (A2aR) in lung tissues of mice and in PASMCs in vitro after hypoxia exposure. Combined the evidence above, we conclude that salidroside can attenuate chronic hypoxia-induced PAH by promoting PASMCs apoptosis via an A2aR related mitochondria dependent pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 82, May 2015, Pages 153-166
Journal: Journal of Molecular and Cellular Cardiology - Volume 82, May 2015, Pages 153-166
نویسندگان
Xiaoying Huang, Lizhen Zou, Xiaoming Yu, Mayun Chen, Rui Guo, Hui Cai, Dan Yao, Xiaomei Xu, Yanfan Chen, Cheng Ding, Xueding Cai, Liangxing Wang,