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. 2017 Dec 5;7:16992. doi: 10.1038/s41598-017-17287-0

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Schematic representation of the protective effect of CP during porcine embryonic development. H₂O₂ exposure causes the generation of oxidative stress, resulting in DNA damage, autophagy, and mitochondrial dysfunction. Apoptosis was induced by the release of cytochrome c from the mitochondria because of the compromise of MMPs. Addition of CP promotes embryo development by attenuating H₂O₂-induced oxidative stress, apoptosis, and compromised MMP because of the antioxidative, anti-apoptosis, and protection mitochondrial dysfunction properties.