氨酸通过Keap1/Nrf2/ARE通路保护衰老的状肌肉免受氧化应激
Ning Gao1, Xiang Gao1, Miaomiao Du1
1The First Affiliated Hospital of Chongqing Medical University, Ophthalmology, Chongqing 400016, PR China; Key Laboratory of Prevention and Treatment on major blinding diseases, Chongqing Eye Institute, Chongqing Branch (Municipality Division) of National Clinical Research Center for Ocular Diseases, Chongqing 400016, PR China.
氨酸补充剂通过减少纤毛肌中的氧化应激来对抗与年龄相关的视力下降. 这项研究表明,黄蛋白通过调节Keap1/Nrf2通路来改善眼睛的适应性和折射误差.
科学领域:
- 眼科医生 眼科 眼科
- 老年学是一门学科.
- 分子生物学分子生物学
背景情况:
- 与年龄相关的纤毛肌功能下降有助于视觉适应缺陷.
- 氧化应激是纤毛肌衰老和视力受损的关键因素.
研究的目的:
- 为了研究黄蛋白对状肌肉中与年龄相关的氧化应激的影响.
- 阐明蛋白对状肌肉功能保护作用的分子机制.
主要方法:
- 实验在体内使用三色几内亚猪进行,在体内使用初级几内亚猪状平滑肌细胞进行.
- 生物信息学分析确定了肌肉衰老与黄蛋白关系中的关键基因,包括Nrf2和抗氧化酶.
- 评估了氨酸对氧化应激标记,衰老,细胞亡,细胞迁移和蛋白质表达的作用.
主要成果:
- 氨酸降低了衰老的肌中的活性氧物种 (ROS) 和P21水平,改善了折射误差和眼睛的适应性.
- 在体外,黄蛋白逆转了H2O2诱导的损伤,减少衰老标志物 (SA-β-Gal,ROS) 和亡,同时增加了收缩性蛋白质.
- 氨酸调节了Keap1/Nrf2通路,增加了抗氧化酶表达 (GPx,SOD,CAT,NQO1,HO-1) 并降低了Keap1水平.
结论:
- 氨酸通过Keap1/Nrf2/Antioxidant Response Element路径增强状肌肉对氧化应激的抵抗力.
- 这项研究证明了黄蛋白的分子机制,可以逆转与年龄相关的状肌肉缩和放缩功能的缺陷.
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