Protective effect of salidroside on cardiac apoptosis in mice with chronic intermittent hypoxia
Protective effect of salidroside on cardiac apoptosis in mice with chronic intermittent hypoxia
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DOI:
10.1016/j.ijcard.2014.04.132
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发表时间:
2014-07-01
影响因子:
3.5
通讯作者:
Lee, Shin-Da
中科院分区:
文献类型:
--
作者:
Lai, Mei-Chih;Lin, Jaung-Geng;Lee, Shin-Da
Background: 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.Methods: Sixty-four C57BL/6 J mice 5-6 months of age were divided into four groups, i.e. Control group (21% O-2, 24 h per day, 8 weeks, n = 16); Hypoxia group (Hypoxia: 7% O-2 60 s, 20% O-2 alternating 60 s, 8 h per day, 8 weeks, n = 16); and Hypoxia + S10 and Hypoxia + S30 groups (Hypoxia for 1st 4 weeks, hypoxia pretreated 10 mg/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.Results: 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.Conclusions: Our findings suggest that salidroside has protective effects on chronic intermittent hypoxia-induced Fas-dependent and mitochondria-dependent apoptotic pathways in mice hearts. (C) 2014 Elsevier Ireland Ltd. All rights reserved.