Inhibition of activated NR2B gene- and caspase-3 protein-expression by glutathione following traumatic brain injury in a rat model

@inproceedings{Arifin2011InhibitionOA,
  title={Inhibition of activated NR2B gene- and caspase-3 protein-expression by glutathione following traumatic brain injury in a rat model},
  author={Muhammad Zafrullah Arifin and Ahmad Faried and Muhammad Nurhalim Shahib and Kahdar Wiriadisastra and Tatang Bisri},
  booktitle={Asian journal of neurosurgery},
  year={2011}
}
BACKGROUND.: Traumatic brain injury (TBI) remains a major cause of death and disability. Oxidative stress is an important element of the injury cascade following TBI. Progressive compromise of antioxidant defenses and free radical-mediated lipid peroxidation are one of the major mechanisms of secondary TBI. NR2B is a glutamate receptor and its activation is caused by TBI increasing a brain cell death, along with caspase-3 as a hall mark of apoptosis. Glutathione is a potent free radical… CONTINUE READING