Protective effect of proanthocyanidin against oxidative ovarian damage induced by 3-nitropropionic acid in mice
文献类型： 外文期刊
作者： Zhang, J. Q. 1 ; Xing, B. S. 2 ; Zhu, C. C. 1 ; Shen, M. 1 ; Yu, F. X. 1 ; Liu, H. L. 1 ;
作者机构： 1.Nanjing Agr Univ, Coll Anim Sci & Technol, Nanjing, Jiangsu, Peoples R China
2.Henan Acad Agr Sci, Inst Anim Husb & Vet Sci, Zhengzhou, Peoples R China
关键词： 3-NPA;Proanthocyanidins;Oxidative stress;Ovary
期刊名称：GENETICS AND MOLECULAR RESEARCH （ 影响因子：0.764； 五年影响因子：0.912 ）
ISSN： 1676-5680
年卷期： 2015 年 14 卷 1 期
页码：
收录情况： SCI
摘要： Oxidative stress, which poses a threat to reproductive health, causes many serious female reproductive diseases. In this study, we investigated whether proanthocyanidins (PC) have a protective effect against oxidative stress-induced ovarian damage. Forty female ICR mice were randomized into 4 groups: a control group, a control plus PC group, a 3-nitropropionic acid (3-NPA) group, and a 3-NPA plus PC group. An ovarian oxidative stress model induced by 3-NPA was constructed using female ICR mice. After the animals were sacrificed, their ovaries were collected to measure reactive oxygen species (ROS) levels, the activities of superoxide dismutase (SOD) and catalase (CAT), and the mRNA expression levels of relevant granulosa cell apoptosis genes (Bcl-2, Bax, Bim, FasL, and caspase-3). We also conducted a histological evaluation of granulosa cell apoptosis and follicular atresia. The results showed that compared to the 3-NPA group, ROS levels and activities of T-SOD and CAT in the 3-NPA plus PC group were significantly decreased (P < 0.05), while the ratio of Bcl-2 to Bax in the 3-NPA plus PC group were significantly increased (P < 0.05). mRNA expression levels of Bim, FasL, and caspase-3 in the 3-NPA plus PC group were significantly decreased (P < 0.05), and the percentage of atretic follicles and granulosa cell apoptosis in the 3-NPA plus PC group was significantly decreased (P < 0.05). Collectively, these data indicate that PC has significant protective effects against damage induced by oxidative stress in mouse ovaries. The mechanisms of protection may be related to antioxidation and apoptosis reduction.
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