Astragalus polysaccharides protect cardiac stem and progenitor cells by the inhibition of oxidative stress-mediated apoptosis in diabetic hearts.

Astragalus polysaccharides protect cardiac stem and progenitor cells by the inhibition of oxidative stress-mediated apoptosis in diabetic hearts.
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DOI:
10.2147/dddt.s155686
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发表时间:
2018
期刊:
Drug design, development and therapy
影响因子:
--
通讯作者:
Zhang Y
Zhang Y
中科院分区:
其他
文献类型:
--
作者:
Chen W;Ju J;Yang Y;Wang H;Chen W;Zhao X;Ye H;Zhang Y

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糖尿病性心肌病的特征在于心肌细胞死亡和再生之间的不平衡,这是由心脏干细胞和祖细胞(CSPC)通过凋亡和坏死的进行性损失介导的,所述凋亡和坏死是由于糖尿病引起的氧化应激的激活。在这项研究中,我们评估了黄芪多糖(APS)治疗对糖尿病心脏CSPC的保护作用,通过其抗氧化能力。采用链脲佐菌素(STZ)诱导的糖尿病小鼠和杂合子(SOD 2 +/−)敲除小鼠,并给予APS。分离心室CSPC用于氧化评价。在心室CSPC的丰度,凋亡和增殖,活性氧(ROS)的形成,氧化损伤,和SOD 2蛋白水平和活性进行了评价。我们证实,APS增加了CSPC的丰度,减少了CSPC的凋亡,并增强了STZ诱导的糖尿病小鼠和非糖尿病SOD 2 +/−小鼠中CSPC的增殖。此外,APS治疗增强了SOD 2蛋白水平和酶活性,并抑制了STZ诱导的糖尿病小鼠和非糖尿病SOD 2 +/−小鼠CSPC的ROS形成和氧化损伤。我们的研究结果表明,APS对糖尿病患者CSPC保存的拯救具有积极作用,依赖于对氧化应激介导的细胞凋亡的抑制。
Diabetic cardiomyopathy is characterized by an imbalance between myocyte death and regeneration mediated by the progressive loss of cardiac stem and progenitor cells (CSPCs) by apoptosis and necrosis due to the activation of oxidative stress with diabetes. In this study, we evaluated the beneficial effect of astragalus polysaccharides (APS) therapy on the protection of CSPCs through its antioxidative capacity in diabetic hearts. Streptozotocin (STZ)-induced diabetic mice and heterozygous (SOD2+/−) knockout mice were employed and administered with APS. Ventricular CSPCs were isolated for oxidative evaluation. The abundance, apoptosis and proliferation, reactive oxygen species (ROS) formation, oxidative damage, and SOD2 protein levels and activities were evaluated in ventricular CSPCs. We confirmed that APS increased the CSPC abundance, reduced the apoptosis of CSPCs, and enhanced the proliferation of CSPCs in both STZ-induced diabetic mice and nondiabetic SOD2+/− mice. In addition, therapy of APS enhanced SOD2 protein levels and enzyme activities, and inhibited ROS formation and oxidative damage of CSPCs from both STZ-induced diabetic mice and nondiabetic SOD2+/− mice. Our findings demonstrated the positive effect of APS on the rescue of CSPC preservation in diabetes, dependent on the inhibition of oxidative stress-mediated apoptosis.