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

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

  • Cell Prolif. 2024 Jun 12:e13687. doi: 10.1111/cpr.13687.
Yuwen Luo 1 2 Jun Li 3 Lv Zheng 1 4 Yizaitiguli Reyimjan 1 4 Yan Ma 1 4 Shuaixiang Huang 1 4 Hongyu Liu 1 4 Guizhen Zhou 1 4 Jiachen Bai 1 4 Yixiao Zhu 1 4 Yidan Sun 1 2 Xinhua Zou 1 4 Yunpeng Hou 1 2 Xiangwei Fu 1 4 5
Affiliations

Affiliations

  • 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

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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