Grape seed proanthocyanidins inhibit H2O2-induced osteoblastic MC3T3-E1 cell apoptosis via ameliorating H2O2-induced mitochondrial dysfunction

被引:53
|
作者
Zhang, Zhifeng [1 ]
Zheng, Leigang [1 ]
Zhao, Zhenqun [1 ]
Shi, Jun [2 ]
Wang, Xing [3 ]
Huang, Jian [1 ]
机构
[1] Inner Mongolia Med Univ, Affiliated Hosp 2, Dept Orthopaed, Hohhot 010030, Peoples R China
[2] Inner Mongolia Med Univ, Dept Basic Med Sci, Teaching & Res Sect Physiol, Hohhot 010110, Peoples R China
[3] Inner Mongolia Med Univ, Dept Basic Med Sci, Teaching & Res Sect Human Anat, Hohhot 010110, Peoples R China
来源
JOURNAL OF TOXICOLOGICAL SCIENCES | 2014年 / 39卷 / 05期
关键词
Proanthocyanidins; MC3T3-E1; cells; Apoptosis; Mitochondrial dysfunction; OXIDATIVE-STRESS; POSTMENOPAUSAL OSTEOPOROSIS; CARDIOMYOCYTE APOPTOSIS; LIPID-PEROXIDATION; REPERFUSION INJURY; NITRIC-OXIDE; BONE; METABOLISM; ACTIVATION; MECHANISMS;
D O I
10.2131/jts.39.803
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
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 resorption 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 proanthocyanidins with their anti-apoptosis effect. Results demonstrated that proanthocyanidins inhibit H2O2-promoted 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 IV, and reducing the mitochondrial free radical production, ROS and mitochondrial 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.
引用
收藏
页码:803 / 813
页数:11
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