Previous studies have demonstrated that lipopolysaccharide (LPS), as a central toxic factor of gram-negative bacteria, can induce oxidative stress and cellular inflammation to result in the impairment of female fertility in different organisms. Particularly, it has harmful effects on the oocyte quality and subsequent embryonic development.However, the approach concerning how to prevent oocytes from LPS-induced deterioration still remains largely unexplored. We assessed the effective influences of velvet antler water extract (VAWE) by immunostaining and fluorescence intensity quantification on the meiotic maturation, mitochondrial function and sperm binding ability of oocytes under oxidative stress. Here, we report that VAWE treatment restores the quality of porcine oocytes exposed to LPS. Specifically, LPS exposure contributed to the failed oocyte maturation, reduced sperm binding ability and fertilization capability by disturbing the dynamics and arrangement of meiotic apparatuses and organelles, including spindle assembly, chromosome alignment, actin polymerization, mitochondrial dynamics and cortical granule distribution, the indicators of oocyte nuclear and cytoplasmic maturation. Notably, VAWE treatment recovered these meiotic defects by removing the LPS-induced excessive ROS and thus inhibiting the apoptosis. Collectively, our study illustrates that VAWE treatment is a feasible strategy to improve the oocyte quality deteriorated by the LPS-induced oxidative stress.
| INTRODUCTIONGram-negative bacteria possess an outer protective cell wall that harbours several pathogen-associated molecular patterns (PAMPs) to trigger the inflammation and cause other toxic effects when they infect a host or are lysed by antibiotics. 1 Lipopolysaccharide (LPS), as a core component of the outer membrane of gram-negative bacteria, exists extensively in numerous industrial and external environments, including livestock farms, lumbermills and cotton mills. 2,3 LPS is a prototypical PAMP which is identified by toll-like receptor 4 (TLR-4) protein in complex with CD14 and soluble myeloid differentiation factor 2 (MD2) on the cell surface. 4,5 After LPS binds to its receptor, inflammatory molecules such as chemokines IL-8, TNF-α, IL-6 and cytokines IL-1β are released. 4 The LPS-induced molecules cause severe pathology by exerting profound regulatory effects on the cellular functions. 6 In addition, many studies have validated the adverse influences of LPS on the folliculogenesis, oocyte development, ovulation, luteal function, ovarian steroidogenesis, estrus behaviour, and puberty onset in female animals. 7 Notably, a recent study has found that exposure to LPS destructed the oocyte meiotic maturation due