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
Lee, Shin-Da
中科院分区:
医学2区
文献类型:
--
作者:
Lai, Mei-Chih;Lin, Jaung-Geng;Lee, Shin-Da

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背景:本研究的目的是确定红景天苷对严重睡眠呼吸暂停模型小鼠缺氧诱导的心脏广泛分散性细胞凋亡是否具有保护作用。方法:将 64 只 5-6 月龄 C57BL/6 J 小鼠分为 4 组,即对照组(21% O-2,每天 24 h,8 周,n = 16);缺氧组(缺氧:7% O-2 60 s,20% O-2 交替 60 s,每天 8 h,8 周,n = 16);缺氧+S10组和缺氧+S30组(缺氧第14周,缺氧预处理,每天口服红景天苷10mg/kg和30mg/kg,第24周,n = 16和16)。对四组离体心脏进行心脏重量指数、H&E染色、TUNEL阳性检测和Western blotting测定。结果:缺氧+S10和缺氧+S30组小鼠心脏中TUNEL阳性凋亡细胞少于缺氧组。与缺氧相比,缺氧+S10和缺氧+S30中Fas配体、Fas死亡受体、Fas相关死亡结构域(FADD)、活化的caspase 8和活化的caspase 3(Fas途径)的蛋白水平降低。在线粒体途径中,缺氧+S10和缺氧+S30中Bclx、Bcl2和Bid(抗凋亡Bcl2家族)的蛋白水平高于缺氧。 Hypoxia+ S10 和 Hypoxia+ S30 中 Bax、t-Bid、活化 caspase 9 和活化 caspase 3 的蛋白水平低于缺氧组。 结论:我们的研究结果表明,红景天苷对慢性间歇性缺氧诱导的小鼠心脏中 Fas 依赖性和线粒体依赖性凋亡途径具有保护作用。 (C) 2014 Elsevier Ireland Ltd. 保留所有权利。
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.