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Schisandrin B enhances embryo competence and potentially mitigates endoplasmic reticulum stress during porcine preimplantation development.
- Source :
-
Theriogenology . May2024, Vol. 220, p26-34. 9p. - Publication Year :
- 2024
-
Abstract
- Endoplasmic reticulum (ER) stress induced by agents such as tunicamycin (TM) substantially impedes the developmental progression of porcine embryos. Lignan compounds such as Schisandrin B (Sch-B), may have the potential to mitigate this stress. However, there are few studies on the effects of Sch-B on embryo development. To address this research gap, this study evaluates the protective efficacy of Sch-B against TM-induced ER stress during pivotal stages of porcine embryogenesis. Notably, embryos treated with Sch-B exhibited pronounced resistance to TM-induced developmental arrest, particularly at the 4-cell stage, facilitating progression to the 8-cell stage and subsequent blastocyst formation. It was also observed that Sch-B effectively reduced reactive oxygen species (ROS) levels and improved mitochondrial membrane potential (MMP). Furthermore, Sch-B positively influenced the expression of several stress-related genes. These findings highlight the promising role of Sch-B in improving porcine embryo development and mitigating ER stress. • Schisandrin B promotes porcine embryonic development by mitigating Tunicamycin-induced 4-cell stage arrest and reducing apoptosis levels in blastocysts. • Schisandrin B mitigates the elevation of reactive oxygen species levels in porcine embryos treated with tunicamycin. • Schisandrin B improves mitochondrial membrane potential in porcine embryos treated with tunicamycin. • Schisandrin B positively influences the expression of several stress-related genes. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 0093691X
- Volume :
- 220
- Database :
- Academic Search Index
- Journal :
- Theriogenology
- Publication Type :
- Academic Journal
- Accession number :
- 176226375
- Full Text :
- https://doi.org/10.1016/j.theriogenology.2024.02.031