Traumatic brain injury (TBI) has become a leading cause of death and disability all over the world. Pharmacological suppression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) can inhibit oxidative stress which is implicated in the pathology of TBI. GSK2795039 was reported to target NOX2 to inhibit [Formula: see text] and ROS production. The present study aimed to investigate the effect of GSK2795039 on NOX2 activity and neurological deficits in a TBI mouse model. TBI mouse model was established by a weight-drop to mouse skull. GSK2795039 at a dose of 100 mg/kg was administrated to mice 30 min before TBI. NOX2 expression and activity were detected by Western blot and biochemical method. Neurological damage and apoptosis were detected by behavioral test and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. GSK2795039 significantly inhibited NOX2 expression and activity in the TBI mouse model. It also attenuated TBI-induced neurological deficits, apoptosis, and neurological recovery. The results indicate that GSK2795039 can be used as a potential drug for TBI treatment.

中文翻译：

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一种有效的NADPH氧化酶2抑制剂在创伤性脑损伤的动物模型中提供了神经保护作用并改善了功能结局。

颅脑外伤（TBI）已成为世界范围内导致死亡和残疾的主要原因。烟酰胺腺嘌呤二核苷酸磷酸酯（NADPH）氧化酶2（NOX2）的药理抑制作用可以抑制氧化应激，这与TBI的病理学有关。据报道，GSK2795039靶向NOX2以抑制[分子式：见正文]和ROS的产生。本研究旨在研究GSK2795039对TBI小鼠模型中NOX2活性和神经功能缺损的影响。TBI小鼠模型是通过对小鼠头骨进行减肥而建立的。在TBI前30分钟将100 mg / kg的GSK2795039给药于小鼠。通过蛋白质印迹和生化方法检测NOX2的表达和活性。通过行为测试和末端脱氧核苷酸转移酶dUTP缺口末端标记染色检测神经损伤和凋亡。GSK2795039在TBI小鼠模型中显着抑制了NOX2的表达和活性。它还减弱了TBI诱导的神经功能缺损，凋亡和神经功能恢复。结果表明，GSK2795039可用作TBI治疗的潜在药物。