한빛사논문
Se‑Been Jeon1,2†, Pil‑Soo Jeong1†, Min Ju Kim1,2, Hyo‑Gu Kang1,3, Bong‑Seok Song1, Sun‑Uk Kim1,4, Seong‑Keun Cho5 and Bo‑Woong Sim1*
1Futuristic Animal Resource & Research Center (FARRC), Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju 28116, Republicof Korea.
2Department of Animal Science, College of Natural Resources & Life Science, Pusan National University, Miryang 50463, Republic of Korea.
3Department of Animal Science and Biotechnology, College of Agriculture and Life Science, Chungnam National University, Daejeon 34134, Republic of Korea.
4Department of Functional Genomics, University of Science and Technology, Daejeon 34113, Republic of Korea.
5Department of Animal Science, Life and Industry Convergence Research Institute (RICRI), College of Natural Resources & Life Science, Pusan National University, Miryang 50463, Republic of Korea.
†Se-Been Jeon and Pil-Soo Jeong contributed equally to this work.
*Correspondence: Bo‑Woong Sim
Abstract
Background: Oxidative stress, caused by an imbalance in the production and elimination of intracellular reactive oxygen species (ROS), has been recognized for its detrimental effects on mammalian embryonic development. Luteolin (Lut) has been documented for its protective effects against oxidative stress in various studies. However, its specific role in embryonic development remains unexplored. This study aims to investigate the influence of Lut on porcine embryonic development and to elucidate the underlying mechanism.
Results: After undergoing parthenogenetic activation (PA) or in vitro fertilization, embryos supplemented with 0.5 µmol/L Lut displayed a significant enhancement in cleavage and blastocyst formation rates, with an increase in total cell numbers and a decrease in the apoptosis rate compared to the control. Measurements on D2 and D6 revealed that embryos with Lut supplementation had lower ROS levels and higher glutathione levels compared to the control. Moreover, Lut supplementation significantly augmented mitochondrial content and membrane potential. Intriguingly, activation of the Nrf2/Keap1 signaling pathway was observed in embryos supplemented with Lut, leading to the upregulation of antioxidant-related gene transcription levels. To further validate the relationship between the Nrf2/Keap1 signaling pathway and effects of Lut in porcine embryonic development, we cultured PA embryos in a medium supplemented with brusatol, with or without the inclusion of Lut. The positive effects of Lut on developmental competence were negated by brusatol treatment.
Conclusions: Our findings indicate that Lut-mediated activation of the Nrf2/Keap1 signaling pathway contributes to the enhanced production of porcine embryos with high developmental competence, and offers insight into the mechanisms regulating early embryonic development.
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