The expression of NF-E2-related factor 2 in the rat brain after traumatic brain injury.

ABSTRACT

BACKGROUND: Secondary brain damage plays a critical role in the outcome of patients with traumatic brain injury (TBI). The mechanisms underlying secondary brain damage are complex. A target that can interrupt multiple mechanisms underlying secondary brain damage may represent a promising new therapeutic approach for TBI. NF-E2-related factor 2 (Nrf2) is the key regulator in reducing oxidative stress, inflammatory damage, and the accumulation of toxic metabolites, which are all involved in secondary brain damage after TBI. Therefore, Nrf2 might represent a new direction for the treatment of TBI. However, the expression pattern of Nrf2 after TBI has not yet been studied. METHODS: This study involved the detection of Nrf2 mRNA levels by reverse-transcriptase polymerase chain reaction, and its nuclear protein levels by Western blot from 3 hour to 72 hour after TBI. Nrf2 distribution in the brain after TBI was also investigated by immunohistochemistry. RESULTS: After TBI, the nuclear Nrf2 protein level is significantly increased, whereas its mRNA level remains unchanged. Increased Nrf2 immunostaining was detected not only in the vulnerable regions but also in the brain barrier system. CONCLUSION: Nrf2 might play a protective role in the brain after TBI, possibly by reducing oxidative stress and brain edema.