Open AccessInhibition of activated NR2B gene- and caspase-3 protein-expression by glutathione following traumatic brain injury in a rat model
Author(s) -
Muhammad Zafrullah Arifin,
Ahmad Faried,
M. Nurhalim Shahib,
Kahdar Wiriadisastra,
Tatang Bisri
Publication year - 2011
Publication title -
europe pmc (pubmed central)
Language(s) - English
Resource type - Journals
eISSN - 2248-9614
DOI - 10.4103/1793-5482.92160
Subject(s) - traumatic brain injury , medicine , glutathione , gene , gene expression , caspase 3 , caspase , protein expression , neuroscience , pharmacology , apoptosis , microbiology and biotechnology , genetics , biochemistry , biology , psychiatry , enzyme , programmed cell death
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 scavenger that might prevent secondary TBI damage and inhibited apoptosis. MATERIALS AND METHODS.: In the present study, it aims to demonstrate the effect of glutathione on inhibition of brain oxidative damage in a TBI rat model. RESULTS.: In this study, the expressions of mRNA NR2B in placebo group and groups with glutathione administration at 0, 3, and 6 hours after TBI were 328.14, 229.90, 178.50, and 136.14, respectively (P<0.001). The highest caspase-3 expression was shown in placebo group with 66.7% showing strong positive results (>80%); as expected, glutathione administered in 0, 3, and 6 hours groups had lower strong positive results of 50%, 16.7%, and 16.7%, respectively, (P=0.025). CONCLUSION.: In conclusion, this study showed that glutathione administration in a TBI rat model decreased NR2B gene- and caspase-3 protein-expression that lead to the inhibition of brain cell death. Our results suggest that glutathione, as a potent free radical scavenger, has a brain cell protective effect against oxidative damage and cell death induced by TBI in rat model.