Inhibition of NOX2 contributes to the therapeutic effect of aloin on traumatic brain injury.

Traumatic brain injury (TBI) is a subset of brain injury induced by external mechanical forces to the head or neck. TBI has been reported to be one of the leading causes of disability, and it causes a huge financial burden around the world. Aloin is the major anthraquinone glycoside extracted from Aloe species, and has presented anti-tumour, anti-oxidative and anti-inflammatory activities. However, few studies have focused the effect of aloin in treatment of TBI. Nicotinamide adenine dinucleotide phosphate oxidase (NOX) is the only subset of enzymes which produces solely the reactive oxygen species (ROS). A recent study showed that activation of NOX might aggravate the primary TBI, and among these members, NOX2 is the key member in regulation of uncontrolled ROS expression, and thus plays a critical role in development of inflammatory diseases. Here, we noticed that inhibition of NOX2 combined with aloin treatment promoted the recovery of brain function in a mice model as well as the viability rate in a cell model. A further study found that the inflammation response process was also inhibited after treatment. Then, we found that these effects might be mediated by the PI3K/AKT/mTOR signalling pathway and NOX2 might be a therapeutic target for TBI.