Role of microglia under cardiac and cerebral ischemia/reperfusion (I/R) injury
© 2018, Springer Science+Business Media, LLC, part of Springer Nature. 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 reperfus...
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Main Authors: | , , , , |
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Format: | Journal |
Published: |
2018
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Subjects: | |
Online Access: | https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85045231896&origin=inward http://cmuir.cmu.ac.th/jspui/handle/6653943832/58213 |
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Institution: | Chiang Mai University |
Summary: | © 2018, Springer Science+Business Media, LLC, part of Springer Nature. 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. |
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