中国神经再生研究(英文版) ›› 2020, Vol. 15 ›› Issue (8): 1388-1396.doi: 10.4103/1673-5374.274331

• 综述:脑损伤修复保护与再生 • 上一篇    下一篇

缺血性卒中时的自噬和炎症

  

  • 出版日期:2020-08-15 发布日期:2020-09-17

Autophagy and inflammation in ischemic stroke

Yun Mo1 , Yin-Yi Sun2 , Kang-Yong Liu3, *   

  1. 1 Department of Neurology, Guizhou Medical University, Guiyang, Guizhou Province, China 2 Department of Neurology, Shanghai Sixth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China 3 Department of Neurology, Shanghai university of medicine & health Sciences Affiliated Zhoupu hospital, Shanghai, China
  • Online:2020-08-15 Published:2020-09-17
  • Contact: Kang-Yong Liu, MD, liukangyong5555@163.com.
  • Supported by:
    This work was supported by the Natural Science Foundation of Shanghai of China, No. 17ZR1425800 (to KYL); the Shanghai Pudong District Health Bureau of China, No. PDZX2017-25 (to KYL).

摘要: orcid: 0000-0003-1678-5212 (Kang-Yong Liu)

Abstract: Appropriate autophagy has protective effects on ischemic nerve tissue, while excessive autophagy may cause cell death. The inflammatory response plays an important role in the survival of nerve cells and the recovery of neural tissue after ischemia. Many studies have found an interaction between autophagy and inflammation in the pathogenesis of ischemic stroke. This study outlines recent advances regarding the role of autophagy in the post-stroke inflammatory response as follows. (1) Autophagy inhibits inflammatory responses caused by ischemic stimulation through mTOR, the AMPK pathway, and inhibition of inflammasome activation. (2) Activation of inflammation triggers the formation of autophagosomes, and the upregulation of autophagy levels is marked by a significant increase in the autophagy-forming markers LC3-II and Beclin-1. Lipopolysaccharide stimulates microglia and inhibits ULK1 activity by direct phosphorylation of p38 MAPK, reducing the flux and autophagy level, thereby inducing inflammatory activity. (3) By blocking the activation of autophagy, the activation of inflammasomes can alleviate cerebral ischemic injury. Autophagy can also regulate the phenotypic alternation of microglia through the nuclear factor-κB pathway, which is beneficial to the recovery of neural tissue after ischemia. Studies have shown that some drugs such as resveratrol can exert neuroprotective effects by regulating the autophagy-inflammatory pathway. These studies suggest that the autophagy-inflammatory pathway may provide a new direction for the treatment of ischemic stroke.

Key words: autophagy, cerebral ischemia, function, inflammasome, inflammation, ischemia/refusion, ischemic stroke, macroautophagy, neuroinflammation, oxygen glucose deprivation