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内质网本身在细胞生理及组成结构方面起至关重要的作用,当内质网出现功能障碍时,未折叠蛋白反应(UPR)试图增加未折叠蛋白的折叠能力而减轻内质网应激(ERS)的压力。当无法缓解时,细胞便通过内质网凋亡途径走向凋亡。而脑缺血/再灌注损伤(CIRI)会导致内环境紊乱,引起ERS反应,进而通过ERS途径引起神经元凋亡。现对内质网的结构、功能、ERS机制、ERS后产生的UPR机制以及凋亡机制予以阐述,并提出了对CIRI后ERS状态下神经元转归的应对措施。
The endoplasmic reticulum itself plays a crucial role in the physiology and composition of the cells, and when the endoplasmic reticulum appears dysfunctional, the unfolded protein reaction (UPR) attempts to increase the folding capacity of the unfolded protein and reduce the endoplasmic reticulum stress ERS) pressure. When unable to alleviate, the cells go apoptosis through the endoplasmic reticulum apoptosis pathway. Cerebral ischemia / reperfusion injury (CIRI) can lead to internal environment disorders, causing ERS response, which in turn leads to neuronal apoptosis through the ERS pathway. The structure, function, ERS mechanism of endoplasmic reticulum, the mechanism of UPR induced by ERS, and the mechanism of apoptosis were elucidated. The response of neuron in ERS after CIRI was proposed.