发光二极管衍生的蓝光过度暴露通过诱导异常ROS积累加速角膜内皮细胞衰老
Zhaolin Liu1, Yiran Yang2, Ke Yan3
1The First Affiliated Hospital, Department of Ophthalmology, Hengyang Medical school, University of South China, Hengyang, Hunan 421001, China; Xiamen University Affiliated Xiamen Eye Center, Fujian Provincial Key Laboratory of Ophthalmology and Visual Science, Fujian Engineering and Research Center of Eye Regenerative Medicine, Eye Institute of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian 361005, China.
Journal of photochemistry and photobiology. B, Biology
|September 7, 2025
概括
蓝光暴露会通过增加角膜内皮细胞 (CEC) 中的氧化应激和细胞损失来加速角膜内皮的衰老. 早期激活Nrf2通路可以提供对这种蓝光引起的损伤的保护作用.
科学领域:
- 眼科医生 眼科 眼科
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 蓝光是可见光谱 (400-500nm) 的高能部分,由于LED的广泛使用,它越来越普遍.
- 角膜内皮细胞 (CEC) 对于保持角膜透明度和清晰视力至关重要.
- 蓝光对CEC和角膜内皮老化的影响尚不清楚.
研究的目的:
- 研究蓝光照射对角膜内皮细胞 (CEC) 的影响.
- 阐明蓝光诱导的角膜内皮老化背后的机制.
主要方法:
- 建立了发光二极管 (LED) 蓝光辐射的体内和体外模型.
- 检查了CEC的命运,包括衰老,功能障碍和亡.
- 评估了氧化应激的指标,重点是活性氧物种 (ROS) 和线粒体功能.
- 研究了Nrf2信号通路的作用.
主要成果:
- 蓝光暴露显著增加了CEC中的ROS产量,导致线粒体氧化应激.
- 这种氧化应激诱导了CEC衰老,功能障碍和细胞亡,加速了角膜内皮的衰老和细胞损失.
- 早期的ROS升高激活了Nrf2信号通路.
- Nrf2通路的激活显示出保护作用,抑制了CEC衰老.
结论:
- 蓝光暴露有助于通过氧化应激和随后的CEC亡导致角膜内皮老化.
- Nrf2信号通路在减轻蓝光引起的CEC损伤方面发挥着保护作用.
- 研究结果提供了关于蓝光相关的角膜衰老机制和潜在的治疗点的见解.
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