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循环中白素-6通过抑制PPARγ通路调解PM_2.5诱导的卵巢损伤

Yingying Chen^1,2, Jinjin Zhang^1,3, Tianyu Zhang^1,3

¹Department of Obstetrics and Gynecology, National Clinical Research Center for Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Research (Washington, D.C.)

|December 6, 2024

概括

空气中的细颗粒物 (PM2.5) 损害了卵巢储备和功能. 洲际蛋白-6 (IL-6) 通过影响卵巢细胞和激素合成来调解这种损伤,从而成为潜在的治疗标.

科学领域:

环境健康环境健康
生殖生物学生殖生物学
毒理学毒理学毒理学

背景情况:

空气中的细颗粒物 (PM2.5) 暴露与降低生育能力和卵巢损伤有关.
驱动PM2.5诱导的卵巢功能障碍的精确机制尚未完全理解.

研究的目的:

阐明PM2.5暴露导致卵巢损伤的机制.
确定PM2.5诱导的生殖损害的关键分子媒介和潜在的治疗点.

主要方法:

利用PM2.5暴露的小鼠模型来评估卵巢储备,激素水平和炎症.
通过重组蛋白干预和中和抗体研究了互白素-6 (IL-6) 的作用.
在实验室中检查IL-6对卵巢theca-interstitial细胞和粒状细胞的影响,包括过氧体增殖器激活受体γ (PPARγ) 途径.
在卵巢过早衰老的患者中分析了循环IL-6水平.

主要成果:

暴露于PM2.5显著降低了卵巢储备,激素水平,并增加了小鼠的卵巢炎症.
在暴露于PM2.5的小鼠中,循环IL-6水平升高,直接介导卵巢损伤.
IL-6向卵巢的theca-interstitial细胞,通过PPARγ通路损害丸激素的合成,导致颗粒细胞的亡和受限的卵泡生长.
在卵巢过早衰老的患者中观察到IL-6水平升高,与卵巢功能相反相关.

结论:

暴露于PM2.5会诱导卵巢功能障碍,主要是通过IL-6介导的机制,准卵巢的theca-interstitial细胞并影响PPARγ通路.
IL-6 作为PM2.5诱导的卵巢损伤的关键调解剂,并代表了与空气污染相关的生殖健康问题的潜在生物标志物和治疗标.

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