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|Title: ||Protective effect of salidroside on cardiac apoptosis in mice with chronic intermittent hypoxia|
|Authors: ||La, Mei-Chih;Lai, Mei-Chih;Jaung-Geng;Lin, Jaung-Geng;Pa, Pei-Ying;Pai, Pei-Ying;La, Mei-Hsin;Lai, Mei-Hsin;Li, Yueh-Min;Lin, Yueh-Min;Yeh, Yu-Lan;Yeh, Yu-Lan;Ch, Shiu-Min;Cheng, Shiu-Min;Liu, Yi-fan;Liu, Yi-fan;黃志揚;HUANG, CHIH-YANG;Lee, Shin-Da;Lee, Shin-Da|
|Keywords: ||Apoptotic;Caspase;Heart;Hypoxia;Low oxygen;Salidroside|
|Issue Date: ||2014-06-04 10:14:45 (UTC+8)|
The goal of this study is to determine if salidroside has protective effects on hypoxia-induced cardiac widely dispersed apoptosis in mice with severe sleep apnea model.
Sixty-four C57BL/6J mice 5-6 months of age were divided into four groups, i.e. Control group (21% O2, 24h per day, 8 weeks, n=16); Hypoxia group (Hypoxia: 7% O2 60s, 20% O2 alternating 60s, 8h per day, 8 weeks, n=16); and Hypoxia+S10 and Hypoxia+S 30 groups (Hypoxia for 1st 4 weeks, hypoxia pretreated 10mg/kg and 30 mg/kg salidroside by oral gavage per day for 2nd 4 weeks, n=16 and 16). The excised hearts from four groups were measured by the heart weight index, H&E staining, TUNEL-positive assays and Western blotting.
TUNEL-positive apoptotic cells in mice heart were less in Hypoxia+S10 and Hypoxia+S30 than those in the Hypoxia group. Compared with Hypoxia, the protein levels of Fas ligand, Fas death receptors, Fas-Associated Death Domain (FADD), activated caspase 8, and activated caspase 3 (Fas pathways) were decreased in Hypoxia+S10 and Hypoxia+S30. In the mitochondria pathway, the protein levels of BcLx, Bcl2, and Bid (anti-apoptotic Bcl2 family) in Hypoxia+S10 and Hypoxia+S30 were more than those in Hypoxia. The protein levels of Bax, t-Bid, activated caspase 9, and activated caspase 3 were less in Hypoxia+S10 and Hypoxia+S30 than those in hypoxia.
Our findings suggest that salidroside has protective effects on chronic intermittent hypoxia-induced Fas-dependent and mitochondria-dependent apoptotic pathways in mice hearts.
Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
|Relation: ||INTERNATIONAL JOURNAL OF CARDIOLOGY;174(3):565-73.|
|Appears in Collections:||[生物科技學系] 期刊論文|
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