Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.
Center of Excellence in Cardiac Electrophysiology, Chiang Mai University, Chiang Mai, 50200, Thailand.
Metab Brain Dis. 2018 Aug;33(4):1019-1030. doi: 10.1007/s11011-018-0232-4. Epub 2018 Apr 14.
Both cerebral and cardiac ischemia causes loss of cerebral blood flow, which may lead to neuronal cell damage, neurocognitive impairment, learning and memory difficulties, neurological deficits, and brain death. Although reperfusion is required immediately to restore the blood supply to the brain, it could lead to several detrimental effects on the brain. Several studies demonstrate that microglia activity increases following cerebral and cardiac ischemic/reperfusion (I/R) injury. However, the effects of microglial activation in the brain following I/R remains unclear. Some reports demonstrated that microglia were involved in neurodegeneration and oxidative stress generation, whilst others showed that microglia did not respond to I/R injury. Moreover, microglia are activated in a time-dependent manner, and in a specific brain region following I/R. Recently, several therapeutic approaches including pharmacological interventions and electroacupuncture showed the beneficial effects, while some interventions such as hyperthermia and hyperoxic resuscitation, demonstrated the deteriorated effects on the microglial activity after I/R. Therefore, the present review summarized and discussed those studies regarding the effects of global and focal cerebral as well as cardiac I/R injury on microglia activation, and the therapeutic interventions.
脑和心脏缺血都会导致脑血流损失,这可能导致神经元细胞损伤、神经认知障碍、学习和记忆困难、神经功能缺损和脑死亡。尽管需要立即再灌注以恢复大脑的血液供应,但这可能会对大脑造成多种有害影响。几项研究表明,脑和心脏缺血/再灌注(I/R)损伤后小胶质细胞的活性增加。然而,I/R 后大脑中小胶质细胞的激活作用尚不清楚。一些报告表明小胶质细胞参与神经退行性变和氧化应激的产生,而另一些报告则表明小胶质细胞对 I/R 损伤没有反应。此外,小胶质细胞在 I/R 后会以时间依赖性的方式在特定的脑区被激活。最近,一些治疗方法,包括药理学干预和电针,显示出了有益的效果,而一些干预措施,如高热和高氧复苏,则显示出对 I/R 后小胶质细胞活性的恶化影响。因此,本综述总结和讨论了关于全脑和局灶性脑以及心脏 I/R 损伤对小胶质细胞激活的影响,以及治疗干预的研究。