کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5971513 | 1576184 | 2014 | 9 صفحه PDF | دانلود رایگان |
BackgroundThe 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.MethodsSixty-four C57BL/6 J mice 5-6 months of age were divided into four groups, i.e. Control group (21% O2, 24 h per day, 8 weeks, n = 16); Hypoxia group (Hypoxia: 7% O2 60 s, 20% O2 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.ResultsTUNEL-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.ConclusionsOur findings suggest that salidroside has protective effects on chronic intermittent hypoxia-induced Fas-dependent and mitochondria-dependent apoptotic pathways in mice hearts.
Journal: International Journal of Cardiology - Volume 174, Issue 3, 1 July 2014, Pages 565-573