Abstract
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.
Highlights
Cerebral ischemia-reperfusion injury (CIRI) is a complex pathophysiological process that can cause severe damage to brain functioning
Significant progress has been made in understanding the pathophysiological mechanisms of cerebral ischemia-reperfusion injury and, at present, the main mechanisms include: energy metabolism disorders, cellular acidosis, synthesis or release of excitotoxic amino acids into doubling, intracellular calcium homeostasis, free radical production, and activation of apoptotic genes (Lin et al, 2016; Figure 1)
The protective effect of IL-6 on cerebral ischemic injury may be related to the following factors: (1) inhibition of the production of IL-1 and tumor necrosis factor (TNF)- α as it stimulates the production of circulating antagonists, such as soluble TNF receptors and IL-1 receptor antagonists, through negative feedback mechanisms; (2) induction of the expression of adrenocorticotropic hormone and hydrocortisone, promoting the expression of acute phase proteins, which have anti-protease and oxygen scavenging effects; and (3) exhibiting endogenous neuroprotection against N-methyl-D-aspartate receptor mediated damage (Fujita et al, 2009)
Summary
Cerebral ischemia-reperfusion injury (CIRI) is a complex pathophysiological process that can cause severe damage to brain functioning. Antioxidation, free radical scavenging, and slowing down oxidative stress have become effective strategies in saving neurons from the pathological processes of cerebral ischemia reperfusion.
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