Procyanidin B2 improves developmental capacity of bovine oocytes via promoting PPARγ/UCP1-mediated uncoupling lipid catabolism during in vitro maturation

文献类型： 外文期刊

第一作者： Luo, Yuwen

作者： Luo, Yuwen;Zheng, Lv;Reyimjan, Yizaitiguli;Ma, Yan;Huang, Shuaixiang;Liu, Hongyu;Zhou, Guizhen;Bai, Jiachen;Zhu, Yixiao;Sun, Yidan;Zou, Xinhua;Hou, Yunpeng;Fu, Xiangwei;Luo, Yuwen;Sun, Yidan;Hou, Yunpeng;Li, Jun;Zheng, Lv;Reyimjan, Yizaitiguli;Ma, Yan;Huang, Shuaixiang;Liu, Hongyu;Zhou, Guizhen;Bai, Jiachen;Zhu, Yixiao;Zou, Xinhua;Fu, Xiangwei;Fu, Xiangwei

作者机构：

期刊名称：CELL PROLIFERATION （ 影响因子：5.9； 五年影响因子：7.3 ）

ISSN： 0960-7722

年卷期： 2024 年

页码：

收录情况： SCI

摘要： Metabolic balance is essential for oocyte maturation and acquisition of developmental capacity. Suboptimal conditions of in vitro cultures would lead to lipid accumulation and finally result in disrupted oocyte metabolism. However, the effect and mechanism underlying lipid catabolism in oocyte development remain elusive currently. In the present study, we observed enhanced developmental capacity in Procyanidin B2 (PCB2) treated oocytes during in vitro maturation. Meanwhile, reduced oxidative stress and declined apoptosis were found in oocytes after PCB2 treatment. Further studies confirmed that oocytes treated with PCB2 preferred to lipids catabolism, leading to a notable decrease in lipid accumulation. Subsequent analyses revealed that mitochondrial uncoupling was involved in lipid catabolism, and suppression of uncoupling protein 1 (UCP1) would abrogate the elevated lipid consumption mediated by PCB2. Notably, we identified peroxisome proliferator-activated receptor gamma (PPAR gamma) as a potential target of PCB2 by docking analysis. Subsequent mechanistic studies revealed that PCB2 improved oocyte development capacity and attenuated oxidative stress by activating PPAR gamma mediated mitochondrial uncoupling. Our findings identify that PCB2 intricately improves oocyte development capacity through targeted activation of the PPAR gamma/UCP1 pathway, fostering uncoupling lipid catabolism while concurrently mitigating oxidative stress.

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