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

IF 5.9 1区 生物学 Q2 CELL BIOLOGY Cell Proliferation Pub Date : 2024-06-12 DOI:10.1111/cpr.13687
Yuwen Luo, Jun Li, Lv Zheng, Yizaitiguli Reyimjan, Yan Ma, Shuaixiang Huang, Hongyu Liu, Guizhen Zhou, Jiachen Bai, Yixiao Zhu, Yidan Sun, Xinhua Zou, Yunpeng Hou, Xiangwei Fu
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Abstract

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 (PPARγ) 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 PPARγ mediated mitochondrial uncoupling. Our findings identify that PCB2 intricately improves oocyte development capacity through targeted activation of the PPARγ/UCP1 pathway, fostering uncoupling lipid catabolism while concurrently mitigating oxidative stress.

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在体外成熟过程中,原花青素 B2 通过促进 PPARγ/UCP1 介导的解偶联脂质分解代谢,提高牛卵母细胞的发育能力。
代谢平衡对卵母细胞的成熟和获得发育能力至关重要。体外培养条件不理想会导致脂质积累,最终导致卵母细胞代谢紊乱。然而,脂质分解在卵母细胞发育过程中的作用和机制目前仍不清楚。在本研究中,我们观察到经过青花素 B2(PCB2)处理的卵母细胞在体外成熟过程中发育能力增强。同时,经 PCB2 处理的卵母细胞氧化应激减少,细胞凋亡下降。进一步的研究证实,经 PCB2 处理的卵母细胞更倾向于脂质分解,导致脂质积累明显减少。随后的分析表明,线粒体解偶联参与了脂质分解代谢,而抑制解偶联蛋白 1(UCP1)将减弱 PCB2 导致的脂质消耗增加。值得注意的是,我们通过对接分析发现过氧化物酶体增殖激活受体γ(PPARγ)是 PCB2 的潜在靶点。随后的机理研究发现,PCB2 通过激活 PPARγ 介导的线粒体解偶联作用,提高了卵母细胞的发育能力并减轻了氧化应激。我们的研究结果表明,PCB2 通过有针对性地激活 PPARγ/UCP1 通路,促进脂质分解代谢的解偶联,同时减轻氧化应激,从而改善卵母细胞的发育能力。
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来源期刊
Cell Proliferation
Cell Proliferation 生物-细胞生物学
CiteScore
14.80
自引率
2.40%
发文量
198
审稿时长
1 months
期刊介绍: Cell Proliferation Focus: Devoted to studies into all aspects of cell proliferation and differentiation. Covers normal and abnormal states. Explores control systems and mechanisms at various levels: inter- and intracellular, molecular, and genetic. Investigates modification by and interactions with chemical and physical agents. Includes mathematical modeling and the development of new techniques. Publication Content: Original research papers Invited review articles Book reviews Letters commenting on previously published papers and/or topics of general interest By organizing the information in this manner, readers can quickly grasp the scope, focus, and publication content of Cell Proliferation.
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