解剖学报 ›› 2018, Vol. 49 ›› Issue (6): 839-845.doi: 10.16098/j.issn.0529-1356.2018.06.025

• 综述 • 上一篇    下一篇

灯盏细辛对视网膜缺氧及其所致炎症损伤保护的研究进展

朱静远 白玉婧 张瑜 吴慧娟*   

  1. 北京大学人民医院眼科,视觉损伤与修复教育部重点实验室,视网膜脉络膜疾病诊治研究北京市重点实验室,北京 100044
  • 收稿日期:2018-01-08 修回日期:2018-02-06 出版日期:2018-12-06 发布日期:2019-02-28
  • 通讯作者: 吴慧娟 E-mail:1411210440@pku.edu.cn
  • 基金资助:
    国家自然科学基金;国家自然科学基金;北京市科技计划项目

Protective effects of erigeron breviscapus on retinal hypoxia and its inflammatory injury

ZHU Jing-yuan BAI Yu-jing ZHANG Yu WU Hui-juan*   

  1. Institute of Ophthalmology, Peking University People’s Hospital, Key Laboratory of Vision Loss and Restoration, Ministry of Education; Beijing Key Laboratory of Diagnosis and Therapy of Retinal and Choroid Diseases, Beijing 100044, China
  • Received:2018-01-08 Revised:2018-02-06 Online:2018-12-06 Published:2019-02-28
  • Contact: WU Hui-juan E-mail:1411210440@pku.edu.cn

摘要:

视网膜缺氧损伤主要是视网膜神经节细胞遭到破坏,如氧化应激、兴奋毒性损伤、炎症损伤等所致。视网膜神经节细胞变性会导致视神经传导功能障碍,故缺氧损伤后短期内阻断视神经细胞损伤通路和增强其存活机制成为恢复视觉的关键。灯盏细辛能通过多种机制对视网膜缺氧损伤起到很好保护作用,其能降低炎症介质的表达,故可通过减轻炎症反应对视网膜缺氧所致的一系列炎症级联效应起到保护作用。

关键词: 灯盏细辛, 视网膜缺氧, 炎症损伤, NLRP3炎症小体, 视神经保护

Abstract:

Retinal hypoxia injury is mainly about the damage of retinal ganglion cells, including oxidative stress, excitotoxicity damage, and inflammatory damage. Degeneration of retinal ganglion cells leads to dysfunction of optic nerve conduction. Therefore, blocking the damage pathways of the optic nerve cells and enhancing their survival mechanisms in the short-term after hypoxic injury becomes the key to restore vision. Erigeron breviscapus can protect the retina from hypoxic injury through a variety of mechanisms. It can reduce the expression of inflammatory mediators, so it can protect a series of inflammatory cascade effects caused by retinal hypoxia by reducing the inflammatory response. The current research progress on the protection of retinal hypoxia and inflammation associated injury with erigeron breviscapus.

Key words: Erigeron breviscapus, Retinal hypoxia, Inflammatory injury, NLRP3 inflammasome, Neuroprotection