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Inflammation and neural repair after ischemic brain injury.
Neurochemistry international ( IF 4.2 ) Pub Date : 2018-10-19 , DOI: 10.1016/j.neuint.2018.10.013
Seiichiro Sakai 1 , Takashi Shichita 1
Affiliation  

Stroke causes neuronal cell death and destruction of neuronal circuits in the brain and spinal cord. Injury to the brain tissue induces sterile inflammation triggered by the extracellular release of endogenous molecules, but cerebral inflammation after stroke is gradually resolved within several days. In this pro-resolving process, inflammatory cells adopt a pro-resolving or repairing phenotype in the injured brain, activating endogenous repairing programs. Although the mechanisms involved in the transition from inflammation to neural repair after stroke remain largely unknown to date, some of the mechanisms for inflammation and neural repair have been clarified in detail. This review focuses on the molecular or cellular mechanisms involved in sterile inflammation and neural repair after stroke. This accumulation of evidence may be helpful for speculating about the endogenous repairing mechanisms in the brain and identifying therapeutic targets for improving the functional prognoses of stroke patients.

中文翻译:

缺血性脑损伤后的炎症和神经修复。

中风会导致神经元细胞死亡,并破坏大脑和脊髓中的神经元回路。对脑组织的损伤诱导了由内源性分子的细胞外释放触发的无菌炎症,但是中风后的脑部炎症在几天之内逐渐消失。在这种促分解过程中,炎性细胞在受伤的大脑中采用促分解或修复表型,从而激活内源性修复程序。迄今为止,尽管从中风后炎症转变为神经修复的机制尚不清楚,但一些炎症和神经修复的机制已得到详细阐明。这篇综述着重于中风后无菌炎症和神经修复所涉及的分子或细胞机制。
更新日期:2018-10-19
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