Following traumatic brain injury (TBI), increased production of reactive oxygen species (ROS) and the ensuing oxidative stress promotes the secondary brain damage that encompasses both grey matter and white matter. As this contributes to the long-term neurological deficits, decreasing oxidative stress during the acute period of TBI is beneficial. While NADPH oxidase (NOX2) is the major producer of ROS, transcription factor Nrf2 that induces antioxidant enzymes promotes efficient ROS disposal. We recently showed that treatment with an antioxidant drug combo of apocynin (NOX2 inhibitor) and TBHQ (Nrf2 activator) protects the grey matter in adult mice subjected to TBI. We currently show that this antioxidant combo therapy given at 2 h and 24 h after TBI also protects white matter in mouse brain. Thus, the better functional outcomes after TBI in the combo therapy treated mice might be due to a combination of sparing both grey matter and white matter. Hence, the antioxidant combo we tested is a potent therapeutic option for translation in future.

创伤性脑损伤 (TBI) 后，活性氧 (ROS) 的产生增加和随之而来的氧化应激促进了包括灰质和白质在内的继发性脑损伤。由于这会导致长期神经功能缺损，因此在 TBI 急性期减少氧化应激是有益的。虽然 NADPH 氧化酶 (NOX2) 是 ROS 的主要产生者，但诱导抗氧化酶的转录因子 Nrf2 可促进有效的 ROS 处理。我们最近表明，用夹竹桃苷（NOX2 抑制剂）和 TBHQ（Nrf2 激活剂）的抗氧化药物组合治疗可以保护接受 TBI 的成年小鼠的灰质。我们目前表明，在 TBI 后 2 小时和 24 小时给予这种抗氧化组合疗法也可以保护小鼠大脑中的白质。因此，在联合治疗治疗的小鼠中，TBI 后更好的功能结果可能是由于同时保留了灰质和白质。因此，我们测试的抗氧化剂组合是未来翻译的有效治疗选择。