Polydatin Attenuates H2O2-Induced Oxidative Stress via PKC Pathway.

Polydatin Attenuates H2O2-Induced Oxidative Stress via PKC Pathway.
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虎杖甙通过 PKC 途径减轻 H2O2 诱导的氧化应激

DOI:
10.1155/2016/5139458
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发表时间:
2016
影响因子:
--
通讯作者:
Li Z
Li Z
中科院分区:
生物学2区
文献类型:
--
作者:
Qiao H;Chen H;Dong Y;Ma H;Zhao G;Tang F;Li Z

文献摘要

相似文献

氧化应激在内皮功能障碍的发病机制中起着重要作用,内皮功能障碍是多种心血管疾病发生的前兆。本研究旨在观察PD对h2o2诱导的人脐静脉内皮细胞(HUVECs)氧化应激损伤(oxidative stress injury, OSI)的保护作用及PD对OSI治疗的可能机制。在没有或存在PD的情况下,HUVECs受到H2O2的影响。结果表明,PD提高了细胞活力、粘附和迁移能力,抑制了乳酸脱氢酶(LDH)和活性氧(ROS)的释放,提高了谷胱甘肽过氧化物酶(GSH-Px)和超氧化物歧化酶(SOD)的含量。TUNEL、荧光检测和Western blot结果显示,OSI上调了细胞凋亡率、caspase-3活性和促凋亡蛋白Bax水平,降低了抗凋亡蛋白Bcl-2水平。然而,PD治疗部分逆转了这些损伤效应,胸腺毒素(THX)激活蛋白激酶C (PKC)反过来消除了PD的抗凋亡作用。此外,PD减弱h2o2诱导的PKCs α和δ磷酸化,增加PKC ε磷酸化。我们的研究结果表明,PD可能通过与PKC通路的多种相互作用来发挥对OSI的保护作用。
Oxidative stress plays an important role in the pathogenesis of endothelial dysfunction, which is found to precede the development of diverse cardiovascular diseases (CVDs). The aim of this study was to observe the protective effects of PD against H2O2-induced oxidative stress injury (OSI) in human umbilical vein endothelial cells (HUVECs) and the possible mechanism of PD in OSI treatment. HUVECs were subjected to H2O2 in the absence or presence of PD. It turned out that PD improved cell viability and adhesive and migratory abilities, inhibited the release of lactate dehydrogenase (LDH) and reactive oxygen species (ROS), and elevated the content of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD). TUNEL, fluorometric assays, and Western blotting showed that OSI upregulated the apoptosis ratio, the activity of caspase-3 and the level of proapoptotic protein Bax and decreased the level of antiapoptotic protein Bcl-2. However, PD treatment partially reversed these damage effects and Protein Kinase C (PKC) activation by thymeleatoxin (THX) in turn eliminated the antiapoptotic effect of PD. Furthermore, PD attenuated the H2O2-induced phosphorylation of PKCs α and δ and increased the phosphorylation of PKC ε. Our results indicated that PD might exert protective effects against OSI through various interactions with PKC pathway.