![]() Inflammation occurs after ischemia-reperfusion injury, which is caused by the dying cells and debris in the absence of microbes. The process of ischemia-reperfusion induces the production of superoxide and nitric oxide from damaged neurons and astrocytes and depletes glutathione, a primary antioxidant to protect against reactive oxygen species-mediated DNA damage. Cerebral ischemia induces large release of glutamate that causes over-activation of NMDA receptors and large inflow of Ca 2+, leading to excitotoxicity-induced cell death. Excitotoxicity, oxidative stress, and inflammation have been considered as major contributors to ischemic neuronal injury. The cellular and molecular mechanisms underlying ischemic stroke-induced brain damage have been extensively investigated. Embolism in brain results in oxygen and glucose deprivation, leading to brain damage and neurologic deficit. Ischemic stroke is caused by arterial embolism and in situ small vessel diseases. Stroke is comprised of ischemic stroke (85%) and hemorrhagic stroke (15%) (intracerebral hemorrhage and subarachnoid hemorrhage)
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