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首页> 外文期刊>The Journal of toxicological sciences >Grape seed proanthocyanidins inhibit H2O2-induced osteoblastic MC3T3-E1 cell apoptosis via ameliorating H2O2-induced mitochondrial dysfunction
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Grape seed proanthocyanidins inhibit H2O2-induced osteoblastic MC3T3-E1 cell apoptosis via ameliorating H2O2-induced mitochondrial dysfunction

机译：葡萄籽原花色素通过改善H2O2引起的线粒体功能障碍来抑制H2O2诱导的成骨细胞MC3T3-E1细胞凋亡

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摘要

Oxidative stress represents a major cause of cellular damage and death in pathological conditions including osteoporosis, in which oxidative stress is associated with increased bone resorp-tion and low bone mass. And grape seed proanthocyanidins are a group of polyphenolic bioflavonoids which are known to possess broad pharmacological activity and therapeutic potential, exerting a protective role against oxidant injury. The aim of our study was to investigate whether proanthocyanidins exert an anti-apoptosis effect in osteoblastic MC3T3-E1 cells, via their antioxidant activity. Firstly, we determined the anti-apoptosis effect of proanthocyanidins in osteoblastic MC3T3-E1 cells, which were subject to H2O2 treatment, then we determined the association of the antioxidant activity exerted by proanthocy-anidins with their anti-apoptosis effect. Results demonstrated that proanthocyanidins inhibit H2O2-pro-moted apoptosis in MC3T3-E1 cells, via ameliorating the viability of MC3T3-E1 cells post H2O2 treatment and reducing the apoptotic cell numbers. And the proanthocyanidins treatment also ameliorates the H2O2-induced mitochondrial dysfunction via promoting the mitochondrial membrane potential (MMP) and respiratory chain complex I V, and reducing the mitochondrial free radical production, ROS and mito-chondrial superoxide. Moreover, the proanthocyanidins inhibit H2O2-induced apoptosis signaling which is mediated by p53. This study implied a possible anti-osteoporosis effect of proanthocyanidins via their antioxidant and anti-apoptosis activity.
机译：氧化应激是导致包括骨质疏松症在内的病理状况中细胞损伤和死亡的主要原因，其中氧化应激与骨吸收增加和骨量低有关。葡萄籽原花色素是一组多酚类生物类黄酮，已知具有广泛的药理活性和治疗潜力，对氧化损伤具有保护作用。我们研究的目的是研究原花青素是否通过抗氧化活性在成骨细胞MC3T3-E1细胞中发挥抗凋亡作用。首先，我们确定了原花青素在接受过氧化氢处理的成骨细胞MC3T3-E1细胞中的抗凋亡作用，然后确定了原花抗生物素所发挥的抗氧化活性与其抗凋亡作用之间的关系。结果表明，原花青素可通过改善H2O2处理后MC3T3-E1细胞的活力并减少凋亡细胞数量来抑制H3O2促进的MC3T3-E1细胞凋亡。原花青素的治疗还通过促进线粒体膜电位（MMP）和呼吸链复合物I V，减少线粒体自由基产生，ROS和线粒体超氧化物，改善了H2O2诱导的线粒体功能障碍。此外，原花青素抑制H 2 O 2诱导的由p53介导的凋亡信号传导。这项研究暗示原花青素通过其抗氧化和抗凋亡活性可能具有抗骨质疏松作用。

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