电脉冲刺激通过Nrf2/抗氧化剂通路保护C2C12细胞管免受过氧化诱导的细胞毒性
Sarah Pribil Pardun1, Anjali Bhat1, Cody P Anderson2
1Department of Anesthesiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Antioxidants (Basel, Switzerland)
|June 27, 2024
概括
电脉冲刺激 (EPS) 通过激活Nrf2通路,增强肌肉细胞的抗氧化防御,从而增加细胞对抗氧化应激的存活率. 这项研究揭示了运动诱导的细胞保护的新机制.
科学领域:
- 肌肉生理学 肌肉生理学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 骨肌肉收缩触发了对运动有益的生化变化.
- 了解运动诱导的适应背后的分子机制至关重要.
研究的目的:
- 研究C2C12神经管中电脉冲刺激 (EPS) 诱导的抗氧化剂适应的机制.
- 阐明反应性氧物种 (ROS) 和线粒体功能在这种适应中的作用.
主要方法:
- 用EPS刺激了C2C12神经管.
- 分析了nrf2和抗氧化酶表达.
- 通过使用MitoSOX-Red,CM-H2DCFDA和EPR光谱测量ROS水平.
- 使用海马和Oroboros评估了线粒体呼吸.
- 细胞活力测试是在过氧化 (H2O2) 暴露下进行的.
主要成果:
- EPS显著上调Nrf2和下游抗氧化酶.
- EPS增加了线粒体和细胞质ROS水平.
- 线粒体最大氧气消耗率和线粒体复合体I/V表达增加.
- 由EPS诱导的抗氧化酶上调持续至少24小时.
- 用EPS治疗的细胞对H2O2诱导的细胞毒性有明显更高的生存率.
结论:
- 通过收缩-线粒体-ROS-Nrf2通路,EPS在C2C12神经管中诱导一种抗氧化预条件作用.
- 这种适应增强了细胞对氧化应激的保护.
- 这些发现提供了关于运动诱导益处的分子基础的见解.
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