Tang Xian Nan, Cairns Belinda, Kim Jong Youl, Yenari Midori A
Department of Neurology, University of California, San Francisco and Veterans Affairs Medical Center, USA.
Neurol Res. 2012 May;34(4):338-45. doi: 10.1179/1743132812Y.0000000021.
Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) was originally identified in immune cells as playing an important microbicidal role. In stroke and cerebrovascular disease, inflammation is increasingly being recognized as contributing negatively to neurological outcome, with NOX as an important source of superoxide. Several labs have now shown that blocking or deleting NOX in the experimental stroke models protects from brain ischemia. Recent work has implicated glucose as an important NOX substrate leading to reperfusion injury, and that NOX inhibition can improve the detrimental effects of hyperglycemia on stroke. NOX inhibition also appears to ameliorate complications of thrombolytic therapy by reducing blood-brain barrier disruption, edema formation, and hemorrhage. Further, NOX from circulating inflammatory cells seems to contribute more to ischemic injury more than NOX generated from endogenous brain residential cells. Several pharmacological inhibitors of NOX are now available. Thus, blocking NOX activation may prove to be a promising treatment for stroke as well as an adjunctive agent to prevent its secondary complications.
烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶（NOX）最初在免疫细胞中被发现具有重要的杀菌作用。在中风和脑血管疾病中，炎症越来越被认为会对神经功能结局产生负面影响，而NOX是超氧化物的重要来源。现在有几个实验室表明，在实验性中风模型中阻断或删除NOX可预防脑缺血。最近的研究表明，葡萄糖是导致再灌注损伤的重要NOX底物，并且抑制NOX可以改善高血糖对中风的有害影响。抑制NOX似乎还可以通过减少血脑屏障破坏、水肿形成和出血来改善溶栓治疗的并发症。此外，循环炎症细胞中的NOX似乎比内源性脑驻留细胞产生的NOX对缺血性损伤的贡献更大。目前有几种NOX的药理抑制剂。因此，阻断NOX激活可能被证明是一种有前途的中风治疗方法，也是预防其继发性并发症的辅助药物。
