Abstract

Early brain injury (EBI), a significant contributor to poor outcome after subarachnoid hemorrhage (SAH), is intimately associated with neuronal apoptosis. Recently, the protective role of hydrogen (H-2) in the brain has been widely studied, but the underlying mechanism remains elusive. Numerous studies have shown nuclear factor-B (NF-kappa B) as a crucial survival pathway in neurons. Here we investigated the role of H-2 in EBI following SAH, focusing on the NF-kappa B pathway. A double blood injection model was used to produce experimental SAH, and H-2-rich saline was injected intraperitoneally. NF-kappa B activity within the occipital cortex was measured. Immunofluorescence was performed to demonstrate the activation of NF-kappa B; Bcl-xL and cleaved caspase-3 were determined via Western blot. Gene expression of Bcl-xL was detected by real-time PCR, and TUNEL and Nissl staining were performed to illustrate brain injury in the occipital cortex. SAH induced a significant increase of cleaved caspase-3. Correspondingly, TUNEL staining demonstrated obvious neuronal apoptosis following SAH. In contrast, H-2 treatment markedly increased NF-kappa B activity and the expression of Bcl-xL and decreased the level of cleaved caspase-3. Additionally, H-2 treatment significantly reduced post-SAH neuronal apoptosis. The current study shows that H-2 treatment alleviates EBI in the rabbits following SAH and that NF-kappa B/Bcl-xL pathway is involved in the protective role of H-2. (c) 2013 Wiley Periodicals, Inc.