Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

神经保护 氧化应激 炎症 缺血 医学 药理学 再灌注损伤 一氧化氮 程序性细胞死亡 脑缺血 脂质过氧化 细胞凋亡 免疫学 内科学 生物 生物化学
作者
Liquan Wu,Xiaoxing Xiong,Xiaomin Wu,Yingze Ye,Zhihong Jian,Zhi Zeng,Lijuan Gu
出处
期刊:Frontiers in Molecular Neuroscience [Frontiers Media SA]
卷期号:13 被引量:218
标识
DOI:10.3389/fnmol.2020.00028
摘要

The cerebral ischemia injury can result in neuronal death and/or functional impairment, which leads to further damage and dysfunction after recovery of blood supply. Cerebral ischemia/reperfusion injury (CIRI) often causes irreversible brain damage and neuronal injury and death, which involves many complex pathological processes including oxidative stress, amino acid toxicity, the release of endogenous substances, inflammation and apoptosis. Oxidative stress and inflammation are interactive and play critical roles in ischemia/reperfusion injury in the brain. Oxidative stress is important in the pathological process of ischemic stroke and is critical for the cascade development of ischemic injury. Oxidative stress is caused by reactive oxygen species (ROS) during cerebral ischemia and is more likely to lead to cell death and ultimately brain death after reperfusion. During reperfusion especially, superoxide anion free radicals, hydroxyl free radicals, and nitric oxide (NO) are produced, which can cause lipid peroxidation, inflammation and cell apoptosis. Inflammation alters the balance between pro-inflammatory and anti-inflammatory factors in cerebral ischemic injury. Inflammatory factors can therefore stimulate or exacerbate inflammation and aggravate ischemic injury. Neuroprotective therapies for various stages of the cerebral ischemia cascade response have received widespread attention. At present, neuroprotective drugs mainly include free radical scavengers, anti-inflammatory agents, and anti-apoptotic agents. However, the molecular mechanisms of the interaction between oxidative stress and inflammation, and their interplay with different types of programmed cell death in ischemia/reperfusion injury are unclear. The development of a suitable method for combination therapy has become a hot topic.
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