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皮质醇阻止了LPS对牛卵细胞成熟的抑制作用 in vitro
Sameera Premaratne1, Mahiro Tamura1, Omowumi Ademola1
1Department of Life and Food Science, Obihiro University of Agriculture and Veterinary Medicine, Hokkaido 080-8555, Japan.
The Journal of reproduction and development
|April 13, 2025
概括
牛卵细胞通过局部皮质醇的产生抵抗脂聚糖 (LPS) 的炎症,这一过程需要孕激素 (P4). 这突显了累积卵细胞复合体 (COC) 对导致不孕症的内毒素的自我保护机制.
科学领域:
- 生殖生物学 生殖生物学
- 内分泌学 在内分泌学.
- 细胞生理学 细胞生理学
背景情况:
- 在周排卵期,在牛的积卵细胞复合体 (COCs) 中,局部皮质醇的产生激增.
- 皮质醇的抗炎性质表明皮质醇对内毒素,如脂多糖 (LPS) 起着保护作用,这可能导致不孕.
- 皮质醇及其与孕激素 (P4) 在卵细胞成熟中的相互作用的确切生理意义尚不清楚.
研究的目的:
- 研究皮质醇和孕激素 (P4) 对受脂聚糖 (LPS) 挑战的牛卵细胞成熟的作用.
- 为了确定局部产生的皮质醇是否可以抵消LPS诱导的卵细胞成熟抑制.
- 阐明孕激素在防治LPS的保护机制中的作用.
主要方法:
- 牛的COCs在体外培养了21小时,具有不同度的LPS,皮质醇,皮质素,三氨酸 (P4合成抑制剂) 和诺米格斯特酸盐 (NA).
- 在不同的治疗条件下评估了卵细胞成熟率.
- 评估了皮质素转化为皮质醇以及P4和NA对LPS作用的影响.
主要成果:
- 根据剂量,LPS抑制了牛卵细胞的成熟,这种效应被皮质醇 (0.1μM) 逆转.
- 牛的COCs将皮质素转化为皮质醇,与内源性皮质醇 (约. 0.01 μM) 减轻LPS影响 (1 μg/ml).
- 孕激素 (P4) 对于卵细胞成熟至关重要,但单独P4或NA并不能阻止LPS抑制;皮质醇对LPS的保护作用需要P4的存在.
结论:
- 牛累积卵细胞复合体 (COCs) 具有一种内在的机制,可以通过局部皮质醇生产来防止LPS诱导的成熟抑制.
- 孕激素 (P4) 对于皮质醇发挥其对LPS的保护功能至关重要.
- 这些发现揭示了皮质醇,孕激素和LPS在维持卵细胞质量和预防不孕症之间复杂的相互作用.
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