Free Radical Damage in Ischemia‐Reperfusion Injury: An Obstacle in Acute Ischemic Stroke after Revascularization Therapy

Abstract

Acute ischemic stroke is a common cause of morbidity and mortality worldwide. Thrombolysis with recombinant tissue plasminogen activator and endovascular thrombectomy are the main revascularization therapies for acute ischemic stroke. However, ischemia-reperfusion injury after revascularization therapy can result in worsening outcomes. Among all possible pathological mechanisms of ischemia-reperfusion injury, free radical damage (mainly oxidative/nitrosative stress injury) has been found to play a key role in the process. Free radicals lead to protein dysfunction, DNA damage, and lipid peroxidation, resulting in cell death. Additionally, free radical damage has a strong connection with inducing hemorrhagic transformation and cerebral edema, which are the major complications of revascularization therapy, and mainly influencing neurological outcomes due to the disruption of the blood-brain barrier. In order to get a better clinical prognosis, more and more studies focus on the pharmaceutical and nonpharmaceutical neuroprotective therapies against free radical damage. This review discusses the pathological mechanisms of free radicals in ischemia-reperfusion injury and adjunctive neuroprotective therapies combined with revascularization therapy against free radical damage.

Role of brain renin angiotensin system in neurodegeneration: An update

“…Studies have shown that brain RAS triggers chronic inflammation leading to the release of ROS and inflammatory mediators through activating glial cells (Carvalho and Moreira, 2018). Uncontrolled effects of these mediators upregulate various inflammatory cascades resulting in cognitive dysfunction and neurodegeneration (Sun et al, 2018;Martire et al, 2015).…”

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