IL-33通过视神经压碎的mTOR/S6信号通路保护视网膜结构和功能
Xinyue Wang1, Jinmiao Li1, Jiahe Nie1
1State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou, 510060, China.
Experimental eye research
|October 14, 2024
概括
介质素-33 (IL-33) 治疗通过激活IL-33/ST2/mTOR/S6通路来保护实验性视觉神经病变中的视觉神经和视网膜,从而提供了一个潜在的治疗策略.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 眼科医生 眼科 眼科
背景情况:
- 视神经病变通过视网膜质细胞损伤和视神经退行导致视力丧失.
- 在视神经损伤中,介质素-33 (IL-33) 和其受体ST2 (IL-33/ST2) 轴的作用仍然在很大程度上未被探索.
研究的目的:
- 阐明IL-33/ST2轴在实验性视神经病变中的功能和分子机制.
- 研究IL-33在保护视神经损伤方面的治疗潜力.
主要方法:
- 在C57BL/6J小鼠中建立了一种视神经粉碎 (ONC) 模型.
- IL-33是通过腹膜内注射的,PBS作为对照.
- 免疫光,qRT-PCR,西部斑,ERG,OCT,H&E和Luxol快速蓝色染色被用于评估分子和结构变化.
主要成果:
- 在ONC后的第3天,IL-33表达达到峰值,与增加的ST2表达相关.
- 治疗IL-33增强了视网膜质细胞的存活率,恢复了视网膜内层的厚度,并减少了视神经的脱髓化.
- 给予IL-33激活了mTOR/S6信号通路,在ONC小鼠中被抑制.
结论:
- 增强IL-33/ST2/mTOR/S6通路可以防止实验性视觉神经病变中的结构和功能损伤.
- IL-33/ST2轴在各种视神经病变中是一个有前途的治疗点.
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