高血糖加重脑缺血损伤机制的研究现状

脑缺血是引起人类死亡的一个重要原因,由于其发病的分子机制十分复杂,各种因子作用相互影响,且多数因子的作用同时存在损伤和保护两种机制,使得脑缺血的研究充满了困难。目前众多研究都证实高血糖对缺血脑组织有损害作用,并可能导致局部或广泛缺血后预后更差。本文依据近几年的实验,重点阐述了五种最新的高血糖加重脑缺血过程和预后损伤的机制假说,包括高血糖通过引起过量谷氨酸释放导致的Ca2^＋大量内流造成损伤、高血糖状态下造成氧化应激从而产生各种自由基对神经元造成损伤、炎症因子相关的损伤、高血糖相关的血液灌流的减少以及高血糖造成脑内酸中毒从而引起损伤。期望这些对机制的探讨能够上加深广大医药研究人员对高血糖加重脑缺血损伤的认识,帮助找到新的药物作用靶点和治疗手段,启发新的研究思路。

Study on the Mechanisms about Hyperglycemia and Brain Injuries after Cerebral Ischemia

Ischemic stroke is a leading cause of death. Since there are too many factors that have been found to be related with the stroke and these factors interact with each other, which factor is the most underlying one is still of no consensus. Recently many researches indicate that hyperglycemia do harm to ischemia tissues, or even make against the prognosis after local or general ischemia. This paper summarizes five potential mechanisms about hyperglycemia and brain injuries based on the recent experiment results, including increase in glutamic-acid-excessive-release-mediated calcium entry into the neurons, glucose-mediated increase in oxidative stress, inflammation-associated injury, poor blood flow to the ischemic penumbra and changes in cerebral metabolism, all of which underlie the injurious effects of hyperglycemia on ischemic stroke. We hope the discussion on these mechanisms will not only help to increase the knowledge of medicinal researchers on hyperglycemia and brain injuries, but also assist them to find effective target, new therapy and other original research thoughts .