氧化应激通过c-Src/VEGF通路破坏透镜上皮细胞之间的连接,参与与年龄相关的白内障形成
Le Zhang1,2, Zi-Feng Zhang1, Yan-Nian Hui1
1Department of Ophthalmology, Eye Institute of PLA, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Current eye research
|December 18, 2023
概括
氧化应激会增加血管内皮生长因子 (VEGF),并破坏与年龄相关的白内障 (ARC) 中的透镜细胞连接. 抑制c-Src/VEGF通路可能会防止白内障的发展.
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:
- 与年龄相关的白内障 (ARC) 是导致视力受损的主要原因.
- 氧化应激与ARC的病变发生有关.
- 血管内皮生长因子 (VEGF) 在ARC病变发生中的作用尚未完全理解.
研究的目的:
- 研究氧化应激对VEGF和透镜上皮细胞连接的影响.
- 探索针对c-Src/VEGF通路用于白内障预防的潜力.
主要方法:
- 人类镜片上皮细胞 (SRA01/04) 和整个小鼠镜片被暴露在过氧化 (H2O2) 中以诱导氧化应激.
- 使用ELISA和免疫光学测量VEGF水平.
- 分析了p-Src,ZO-1和N-cadherin的表达方式,这些表达方式是用西方斑点和免疫光学分析.
- 包括Catalase (CAT),PP1和Avastin在内的抑制剂被用来阻止特定的途径.
主要成果:
- 在ARC患者和H2O2治疗细胞中,VEGF分泌和表达升高.
- 氧化应激导致p-Src和VEGF的增加,并减少ZO-1和N-cadherin.
- CAT有效地阻断了H2O2诱导的变化;PP1抑制了c-Src/VEGF;阿瓦斯部分抑制了VEGF.
- 抑制剂在H2O2诱导的小鼠透镜中部分阻止了白内障的形成.
结论:
- 氧化应激激活c-Src/VEGF通路,破坏镜片上皮细胞连接.
- 抑制这种途径显示出预防或治疗与年龄相关的白内障的潜力.
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