Han Hyung Soo, Yenari Midori A
Department of Physiology, Kyungpook National University School of Medicine, Daegu, Korea.
Curr Opin Investig Drugs. 2003 May;4(5):522-9.
Ischemia elicits an inflammatory response in the injured brain that is mediated by various factors, leading to the accumulation of inflammatory cells. These cells, in turn, generate both toxic and reparative substances. The inflammatory reaction, which has a rapid onset and continues after the stroke, is thought to acutely contribute to the evolution of tissue injury. Knowledge of these signaling pathways has led to the identification of a variety of therapeutic targets for stroke treatment, particularly during the reperfusion phase. Whether these targets will be useful in the development of therapies for the treatment of stroke in humans is far from clear, but they provide fertile ground for scientific investigation.
缺血会在受损大脑中引发炎症反应,该反应由多种因素介导,导致炎症细胞积聚。反过来,这些细胞会产生有毒和修复性物质。这种炎症反应起病迅速,中风后仍会持续,被认为会急性促进组织损伤的发展。对这些信号通路的了解已促成了多种中风治疗靶点的识别,尤其是在再灌注阶段。这些靶点是否会对人类中风治疗疗法的开发有用还远未明确,但它们为科学研究提供了丰富的素材。