通过α7nAChR/Nrf2/HO-1信号通路调节微质的M1/M2极化,SAM可以缓解神经炎症
Kang Ma1, Jiandong Niu2, Liang Zeng2
1School of Basic Medicine, Qingdao University, 308 Ningxia Road, Qingdao, Shandong Province, 266071, China.
通过防止微质激活,S-adenosylmethionine (SAM) 降低了与衰老相关的神经炎症. 通过α7nAChR/Nrf2/HO-1通路,SAM通过α7nAChR/Nrf2/HO-1通路促进从促炎M1转向抗炎M2微质的转变.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 衰老研究研究 衰老研究
背景情况:
- 微质细胞是神经炎症的关键驱动因素,在衰老病原发生过程中发挥着关键作用.
- 在衰老过程中微质激活的精确机制仍然不完全理解.
- 调查S-adenosylmethionine (SAM) 在调节衰老期间微质激活中的作用至关重要.
研究的目的:
- 研究SAM对D-银糖诱导的微质衰老和激活的影响.
- 阐明SAM在微质上作用的分子机制.
- 为了确定SAM是否通过抑制微质极化来减轻神经炎症.
主要方法:
- 使用BV2细胞用D-银糖 (D-gal) 处理,以模拟与衰老相关的微质激活.
- 使用的细胞计数工具-8 (CCK8) 测定,与衰老相关的β-Galactosidase (SA-β-gal) 染色,西斑和免疫光.
- 研究了α7尼古丁性乙胆受体 (α7nAChR) 途径的作用,使用选择性抗剂 (甲基利卡尼丁酸盐,MLA).
主要成果:
- D-银河糖诱导的微质衰老. D-银河糖诱导的微质衰老.
- 在SAM干预中,促炎标记物 (iNOS,TNF-α,IL-1β) 降低,抗炎标记物 (Arg1,α7nAChR,Nrf2,HO-1) 增加.
- SAM促进了M1到M2微质的两极分化,抑制了促炎性细胞因子,并上调了α7nAChR,Nrf2和HO-1,这种效应部分依赖于α7nAChR信号传递.
结论:
- SAM有效地减轻D-银糖诱导的小质衰老和神经炎症.
- 萨姆抑制微质偏向向一个亲炎性M1表型.
- 萨姆的神经保护作用通过α7nAChR/Nrf2/HO-1信号通路进行介导,突出其在与衰老相关的神经炎症的治疗潜力.
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