Zhang J Q, Xing B S, Zhu C C, Shen M, Yu F X, Liu H L
College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, Jiangsu, China.
Institute of Animal Husbandry and Veterinary Science, Henan Academy of Agricultural Sciences, Zhengzhou, China.
Genet Mol Res. 2015 Mar 30;14(1):2484-94. doi: 10.4238/2015.March.30.6.
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.
氧化应激对生殖健康构成威胁,会引发许多严重的女性生殖疾病。在本研究中,我们调查了原花青素(PC)是否对氧化应激诱导的卵巢损伤具有保护作用。将40只雌性ICR小鼠随机分为4组:对照组、对照加PC组、3-硝基丙酸(3-NPA)组和3-NPA加PC组。使用雌性ICR小鼠构建由3-NPA诱导的卵巢氧化应激模型。处死动物后,收集其卵巢以测量活性氧(ROS)水平、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性,以及相关颗粒细胞凋亡基因(Bcl-2、Bax、Bim、FasL和caspase-3)的mRNA表达水平。我们还对颗粒细胞凋亡和卵泡闭锁进行了组织学评估。结果显示,与3-NPA组相比,3-NPA加PC组的ROS水平以及T-SOD和CAT的活性显著降低(P<0.05),而3-NPA加PC组中Bcl-2与Bax的比值显著升高(P<0.05)。3-NPA加PC组中Bim、FasL和caspase-3的mRNA表达水平显著降低(P<0.05),并且3-NPA加PC组中闭锁卵泡和颗粒细胞凋亡的百分比显著降低(P<0.05)。总体而言,这些数据表明PC对小鼠卵巢氧化应激诱导的损伤具有显著的保护作用。其保护机制可能与抗氧化和减少细胞凋亡有关。