Protective effects of timosaponin B-II on high glucose-induced apoptosis in human umbilical vein endothelial cells

Protective effects of timosaponin B-II on high glucose-induced apoptosis in human umbilical vein endothelial cells
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DOI:
10.1016/j.etap.2013.11.009
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发表时间:
2014-01-01
影响因子:
4.3
通讯作者:
Yang, Zhonglin
Yang, Zhonglin
中科院分区:
环境科学与生态学3区
文献类型:
--
作者:
Guo, Changrun;Li, Lu;Yang, Zhonglin

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本研究旨在探讨知母中的主要生物活性成分知母皂苷B-II对高糖诱导的人脐静脉内皮细胞(HUVECs)的细胞毒性和细胞凋亡的保护作用及其可能的机制。结果表明,与正常对照组相比,高糖培养72 h后,HUVECs乳酸脱氢酶释放、活性氧产生、Caspase-3活性和细胞凋亡率均显著增加(p<0.01)。而预先给予硫代皂苷B-II后,细胞存活率显著增加,乳酸脱氢酶释放量、Caspase-3活性和细胞凋亡率呈浓度依赖性下降(p<0.05)。此外,硫代皂苷B-II还能显著降低心肌组织中的活性氧含量和丙二醛含量,促进谷胱甘肽过氧化物酶活性、内皮型一氧化氮合酶活性和一氧化氮释放(p<0.05)。提示硫代皂苷B-II通过抑制高糖诱导的氧化应激抑制内皮细胞的凋亡,具有预防糖尿病心血管并发症的潜力。(C)2013爱思唯尔B.V.保留所有权利。
This study was designed to investigate the action of timosaponin B-II, a main bioactive compound in Anemarrhena asphodeloides Bunge, on the prevention from high glucose-induced cytotoxicity and apoptosis in human umbilical vein endothelial cells (HUVECs) and the potential mechanisms involved. The results showed that compared with the normal control group, exposure of HUVECs to high glucose media for 72 h resulted in a significant increase in lactates dehydrogenise release, reactive oxygen species production, Caspase-3 activity and the percentage of apoptotic cells (p < 0.01). However, pretreatment with timosaponin B-II significantly increased the viability of HUVECs and decreased lactates dehydrogenise release, Caspase-3 activity and the apoptosis rate in a concentration-dependent manner (p < 0.05). In addition, timosaponin B-II notably decreased the amount of reactive oxygen species and malondialdehyde, as well as promoted glutathione peroxidase activity, endothelial nitric oxide synthase activity and nitric oxide release (p < 0.05). These results suggest that timosaponin B-II has the antiapoptotic effect in endothelial cells through inhibition of high glucose-induced oxidative stress and has the potential for preventing diabetic cardiovascular complications. (C) 2013 Elsevier B.V. All rights reserved.