Inflammation and neural repair after ischemic brain injury
Inflammation and neural repair after ischemic brain injury
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DOI：
10.1016/j.neuint.2018.10.013
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发表时间：
2019-11-01
影响因子：
4.2
通讯作者：
Shichita, Takashi
中科院分区：
文献类型：
--
作者：
Sakai, Seiichiro;Shichita, Takashi
中风导致脑和脊髓中的神经元细胞死亡和神经元回路的破坏。脑组织的损伤诱导由内源性分子的细胞外释放触发的无菌性炎症，但中风后的脑炎症在几天内逐渐消退。在这个促消退过程中，炎性细胞在受损的大脑中采用促消退或修复表型，激活内源性修复程序。虽然涉及中风后从炎症到神经修复的转变的机制迄今为止在很大程度上仍然未知，但炎症和神经修复的一些机制已经详细阐明。本文综述了卒中后无菌性炎症和神经修复的分子或细胞机制。这些证据的积累可能有助于推测脑内内源性修复机制，并确定改善脑卒中患者功能障碍的治疗靶点。
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.