神经炎症
NADPH氧化酶
氧化应激
烟酰胺腺嘌呤二核苷酸磷酸
小胶质细胞
缺血
药理学
医学
炎症
化学
免疫学
内科学
生物化学
氧化酶试验
酶
作者
Qiqi Li,Jiaying Li,Ming Zhou,Zheng‐Hong Qin,Rui Sheng
标识
DOI:10.1016/j.neuint.2021.105081
摘要
Cerebral ischemia is a disease of ischemic necrosis of brain tissue caused by intracranial artery stenosis or occlusion and cerebral artery embolization. Neuroinflammation plays an important role in the pathophysiology of cerebral ischemia. Microglia, astrocytes, leukocytes and other cells that release a variety of inflammatory factors involved in neuroinflammation may play a damaging or protective role during the process of cerebral ischemia. TP53-induced glycolysis and apoptotic regulators (TIGAR) may facilitate the production of nicotinamide adenine dinucleotide phosphoric acid (NADPH) via the pentose phosphate pathway (PPP) to inhibit oxidative stress and neuroinflammation. TIGAR can also directly inhibit NF-κB to inhibit neuroinflammation. TIGAR thus protect against cerebral ischemic injury. Exogenous NADPH can inhibit neuroinflammation by inhibiting oxidative stress and regulating a variety of signals. However, since NADPH oxidase (NOX) may use NADPH as a substrate to generate reactive oxygen species (ROS) to mediate neuroinflammation, the combination of NADPH and NOX inhibitors may produce more powerful anti-neuroinflammatory effects. Here, we review the cells and regulatory signals involved in neuroinflammation during cerebral ischemia, and discuss the possible mechanisms of targeting neuroinflammation in the treatment of cerebral ischemia with TIGAR/NADPH axis, so as to provide new ideas for the prevention and treatment of cerebral ischemia.
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