炎症诱导的LncRNA SNHG1通过IL-17 A信号通路在非阻塞性亚精中协调精子的发育
Yongtong Zhu1, Maocai Li1, Xiaomin Zhan1
1Department of Obstetrics and Gynecology, Center for Reproductive Medicine, Nanfang Hospital, Southern Medical University, 1838 Guangzhou North Avenue, Guangzhou, 510515, Guangdong, China.
Cellular and molecular life sciences : CMLS
|January 6, 2026
概括
非阻塞性亚精精子症 (NOA) 涉及炎症. 这项研究揭示了SP1-SNHG1-IL-17A通路驱动NOA的炎症性精子发生失败,这表明IL-17A抑制是治疗策略.
科学领域:
- 生殖生物学 生殖生物学
- 分子内分泌学分子内分泌学
- 炎症研究 炎症研究
背景情况:
- 非阻塞性精症 (NOA) 是男性不孕症的主要原因之一,与炎症有关.
- 在NOA中炎症损伤的精确分子机制仍然不清楚.
研究的目的:
- 为了研究长非编码RNA SNHG1在NOA病变发生过程中的作用.
- 阐明涉及炎症性精子生成失败的分子轴.
主要方法:
- 利用了脂聚糖 (LPS) 诱导的炎小鼠模型和精子细胞系 (GC-1 spg,TCAM-2).
- 评估了SNHG1和SP1表达,SP1-SNHG1促进体结合,以及通过RNA-seq.激活IL-17A信号通路.
- 采用IL-17A受体阻断剂 (Brodalumab) 来评估功能影响.
主要成果:
- 在NOA模型中,SNHG1和SP1被上调,与精子质功能障碍相关.
- SP1直接激活了SNHG1转录;SNHG1敲击改善了LPS诱导的损伤.
- 过度表达SNHG1激活了IL-17A通路,而IL-17A受体阻断逆转了SNHG1诱导的影响.
结论:
- SP1-SNHG1-IL-17A轴驱动非阻塞性亚精中炎症性精子生成失败.
- 准IL-17A通路为NOA提供了一个潜在的治疗途径.
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