Traumatic brain injury is caused by physical collision (primary injury). It changes the brain’s biochemistry and disturbs the normal brain function such as memory loss and consciousness disturbance (secondary injury). The severity can be measured with the Glasgow Coma Scale. The secondary injury will cause oxidative stress that leads to the nervous cells death, so treatment is needed before it gets worse. Primary injury results in excess of reactive oxidative stress (ROS) which is known from NADPH oxidase 2 (Nox2). Excessive ROS is deadly to the nerve cells. Excessive ROS will activate nuclear factor erythroid 2-like 2 (Nrf2). Nrf2 will bind to antioxidant response elements, to protect multi organs against ROS, including this brain injury. However, this does not last long, so it requires handling excess ROS. can inhibit the activation of Nox2, and reduce the neuron injuries in the hippocampus. It also protects the tissues from oxidative stress. While Nrf2 can be activated by , to protect cells. The combination may reduce the secondary brain injury, improve the neurologic recovery, cognitive function, and reduce the secondary cortical lesion.Copyright: © 2020 Asian Journal of Neurosurgery.
Combined Therapy Potential of Apocynin and Tert-butylhydroquinone as a Therapeutic Agent to Prevent Secondary Progression to Traumatic Brain Injury.
