Pradoldej SompolYong XuWanida IttaratChotiros DaosukhoDaret St. ClairUniversity of Kentucky College of MedicineMahidol University2018-08-202018-08-202006-07-01Journal of Molecular Neuroscience. Vol.29, No.3 (2006), 279-288089586962-s2.0-33750589672https://repository.li.mahidol.ac.th/handle/123456789/23883Expression of manganese superoxide dismutase (MnSOD), a nuclear-encoded mitochondrial primary antioxidant enzyme, is protective against various paradigms of oxidative stress-induced brain injury. We have shown previously that the presence of an intronic nuclear factor site, κB (NF-κB), in the MnSOD gene is essential for the induction of MnSOD by tumor necrosis factor α (TNF-α). However, whether activation of NF-κB is protective against oxidative stress-induced neuronal injury is unclear. In the present study, we demonstrate that TNF-α activates NF-κB activity in neuronal, SH-SY5Y, cells and preferentially enhances the binding of p50 and p65 to the promoter/enhancer regions of the MnSOD gene. Binding of NF-κB members to the MnSOD gene leads to the induction of MnSOD mRNA and protein levels. Consequently, induction of MnSOD by TNF-α primes neuronal cells to develop resistance against subsequent exposure to β-amyloid and FeSO4. Taken together, these results suggest that NF-κB might exert its protective function by induction of MnSOD leading to subsequent protection against oxidative stress-induced neuronal injury. Copyright © 2006 Humana Press Inc.Mahidol UniversityNeuroscienceArticleSCOPUS10.1385/JMN:29:3:279