在中风小鼠中,CircFndc3b通过ENO1/KLF2轴通过缓解微质/巨质烧亡来调解运动诱导的神经保护
Yun Zhao1,2, Xiaofei He1, Xiaofeng Yang1
1Department of Rehabilitation Medicine, The Third Affiliated Hospital, Sun Yat-sen University, 600 Tianhe Road, Guangzhou, Guangdong, 510630, China.
Advanced science (Weinheim, Baden-Wurttemberg, Germany)
|October 28, 2024
概括
运动通过调节circFndc3b,一种循环RNA,抑制大脑中有害的炎症和细胞死亡,从而增强缺血性中风后的神经保护. 这一发现揭示了中风恢复的新治疗点.
科学领域:
- 神经科学是一个神经科学.
- 分子生物学分子生物学
- 遗传学 遗传学 是一个
背景情况:
- 缺血性中风会导致严重的神经损伤.
- 众所周知,运动可以减轻中风后的神经功能障碍.
- 循环RNAs (circRNAs) 在运动诱导的神经保护中的作用尚不清楚.
研究的目的:
- 调查 circFndc3b 在缺血性中风后运动介导的神经保护中的作用.
- 阐明circFndc3b发挥神经保护作用的分子机制.
主要方法:
- 利用中脑动脉阻塞 (MCAO) 缺血性中风的小鼠模型.
- 分析了半皮质中的circFndc3b表达.
- 研究了circFndc3b与伊诺酶1 (ENO1),克鲁佩尔样因子2 (Klf2) mRNA和化在肉瘤 (FUS) mRNA的相互作用.
- 评估了热,心脏病发作量和神经恢复.
主要成果:
- 在MCAO小鼠中,circFndc3b的下调,但在微质/巨细胞中通过炼而上调.
- 运动诱导的circFndc3b缓解了热,减少了心脏病发作量,并改善了神经恢复.
- circFndc3b通过ENO1稳定了Klf2mRNA,抑制了NLRP3炎症酶介导的烧灭.
- 确定了涉及circFndc3b,ENO1和FUS的积极反循环,增强了circFndc3b的表达.
结论:
- circFndc3b通过ENO1/Klf2通路调解运动诱导的抗火虫效应.
- 一个circFndc3b/ENO1/FUS反循环增强了运动的神经保护效益.
- circFndc3b是治疗缺血性中风的新型治疗点.
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