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

Author:

Luo Yuwen12,Li Jun3ORCID,Zheng Lv14,Reyimjan Yizaitiguli14,Ma Yan14,Huang Shuaixiang14,Liu Hongyu14,Zhou Guizhen14,Bai Jiachen14,Zhu Yixiao14,Sun Yidan12,Zou Xinhua14,Hou Yunpeng12ORCID,Fu Xiangwei145ORCID

Affiliation:

1. State Key Laboratory of Animal Biotech Breeding China Agricultural University Beijing China

2. College of Biological Sciences China Agricultural University Beijing China

3. Department of Reproductive Medicine, Reproductive Medical Center The First Hospital of Hebei Medical University Shijiazhuang Hebei China

4. National Engineering Laboratory for Animal Breeding, Key Laboratory of Animal Genetics, Breeding and Reproduction of the MARA, Beijing Key Laboratory for Animal Genetic Improvement, College of Animal Science and Technology China Agricultural University Beijing China

5. State Key Laboratory of Sheep Genetic Improvement and Healthy Breeding Xinjiang Academy of Agricultural and Reclamation Sciences Shihezi, Xinjiang China

Abstract

AbstractMetabolic 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.

Funder

Natural Science Foundation of Hebei Province

National Key Research and Development Program of China

Publisher

Wiley

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