脑缺血再灌注损伤的潜在机制和途径:治疗性GLANCE。

Q3 Medicine
Acta neurologica Taiwanica Pub Date : 2019-12-15
Fatemeh Amini, Zeinab Deris Zayeri, Khojasteh Hoseiny Nejad
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引用次数: 0

摘要

脑缺血再灌注损伤是一种进行性疾病,由于血流障碍导致神经元细胞代谢所需的氧气和营养物质缺乏。这种疾病的发病机制不同;然而,研究表明,炎症的发生通过活性氧的产生与I/R相互作用,并增加神经细胞的凋亡。因此,不同的信号通路会干扰炎症的诱导和活性氧的产生。因此,这些途径的共同点是导致凋亡诱导分子的出现,抑制抗凋亡分子如BCL-2的表达。另一方面,由于其中一些通路在细胞凋亡和血管生成中具有双重作用,因此可以说,进一步的研究可以有助于根据脑缺血再灌注损伤诱导血管生成的发病机制找到合适的治疗策略,以修复受损静脉,防止疾病进展。关键词:再灌注;一氧化氮;活性氧;疗法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Potential Mechanism and Pathways in Cerebral Ischemia- Reperfusion Injury: Therapeutic GLANCE.

Abtract Cerebral ischemia-reperfusion injury is a progressive disease that results in the lack of oxygen and nutrients needed for cellular metabolism in neurons due to blood flow disorders. The pathogenesis of this disease is different; however, it has been shown that the onset of inflammation interacts with I/R through the production of active oxygen species and increases the apoptosis of the neural cells. Therefore, different signaling pathways interfere with the induction of inflammation and the production of active oxygen species. Therefore, the common point of these pathways leads to the appearance of apotosisinducing molecules and inhibit the expression of anti-apoptosis molecules such as BCL-2. In the other hand, due to the dual role of some of these pathways in apoptosis and angiogenesis, it can be said that further studies can be useful in finding suitable therapeutic strategies based on the pathogenesis of Cerebral ischemia-reperfusion injury inducing angiogenesis in order to repair damaged veins and prevent disease progression. Keywords: Reperfusion; Nitric Oxide; Reactive Oxygen Species; Therapeutics.

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来源期刊
Acta neurologica Taiwanica
Acta neurologica Taiwanica Medicine-Neurology (clinical)
CiteScore
1.30
自引率
0.00%
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