Abstract
Accumulating evidence has demonstrated that lipopolysaccharide (LPS) compromises female reproduction, especially oocyte maturation and competence. However, methods to protect oocyte quality from LPS-induced deterioration remain largely unexplored. We previously found that mogroside V (MV) can promote oocyte maturation and embryonic development. However, whether MV can alleviate the adverse effects of LPS exposure on oocyte maturation is unclear. Thus, in this study, we used porcine oocytes as a model to explore the effects of MV administration on LPS-induced oocyte meiotic defects. Our findings show that supplementation with MV protected oocytes from the LPS-mediated reduction in the meiotic maturation rate and the subsequent blastocyst formation rate. In addition, MV alleviated the abnormalities in spindle formation and chromosome alignment, decrease in α-tubulin acetylation levels, the disruption of actin polymerization, and the reductions in mitochondrial contents and lipid droplet contents caused by LPS exposure. Meanwhile, LPS reduced m6A levels in oocytes, but MV restored these epigenetic modifications. Furthermore, MV reduced reactive oxygen species (ROS) levels and early apoptosis in oocytes exposed to LPS. In summary, our study demonstrates that MV can protect oocytes from LPS-induced meiotic defects in part by reducing oxidative stress and maintaining m6A levels.
Highlights
Lipopolysaccharide (LPS), the main component of the outer membrane of the cell wall in gramnegative bacteria, is a typical pathogen-associated molecular pattern (PAMP), known as an endotoxin (Bidne et al, 2018)
Because the polar body extrusion (PBE) ratio in the 15 μg/mL LPS-exposed oocytes (LPS) + 50 μM mogroside V (MV) group were close to the control group, these concentrations were used in the subsequent experiments
The results indicate that MV supplementation protects against oocyte meiotic maturation failure and embryonic developmental arrest caused by LPS exposure
Summary
Lipopolysaccharide (LPS), the main component of the outer membrane of the cell wall in gramnegative bacteria, is a typical pathogen-associated molecular pattern (PAMP), known as an endotoxin (Bidne et al, 2018). As a type of PAMP, LPS is recognized by immunocytes and promotes the release of cytokines, which can lead to systemic inflammation, multiple-organ dysfunction syndrome, endotoxemia, and septic shock (Cavaillon, 2018). LPS adversely affects female reproduction; for example, it inhibits the secretion of reproductive hormones, disturbs the regulation of follicular activation, and reduces the primordial follicular pool reserve (Bromfield and Sheldon, 2013; Magata et al, 2014; Bidne et al, 2018). It is shown that LPS severely affects physiological health and female reproductive performance.
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