Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, 1501 Kings Hwy, Shreveport, LA, USA.
Curr Med Chem. 2014;21(19):2130-7. doi: 10.2174/0929867321666131228192119.
Ischemic stroke remains a leading cause of death worldwide. While the underlying causes of stroke remain poorly defined, brain inflammation appears to be a characteristic response to the vascular insult and there is growing evidence suggesting a cause-effect relationship between the inflammatory response and stroke-induced brain dysfunction and tissue injury. In this review, we summarize evidence that implicates leukocytes in the pathophysiology of stroke and address some of the mediators that contribute to the recruitment and activation of leukocytes in the post-ischemic brain. The products of leukocyte activation that may account for the deleterious effects of this cell population in stroke is also discussed. Recently tested compounds that afford protection against the neurological deficits and tissue injury induced by stroke are addressed within the context of potential development of novel strategies for stroke treatment.
缺血性脑卒中仍然是全球范围内的主要致死原因。尽管脑卒中的根本病因仍未得到明确界定，但脑内炎症似乎是对血管损伤的一种特征性反应，越来越多的证据表明，炎症反应与脑卒中引起的脑功能障碍和组织损伤之间存在因果关系。在这篇综述中，我们总结了白细胞在脑卒中病理生理学中的作用，并探讨了一些介导物，这些介导物有助于在缺血性脑卒中后募集和激活白细胞。本文还讨论了可能导致这种细胞群体在脑卒中时产生有害作用的白细胞激活产物。在探讨新的脑卒中治疗策略的背景下，本文还涉及了最近针对脑卒中引起的神经功能缺损和组织损伤的保护化合物。
