Xifeng Wang1, Lianshuang Zhang2, Wei Zhao2, Tongshen Liu2. 1. Department of Critical Care Medicine, Yu Huang Ding Hospital, Qingdao University, Yan Tai, P.R. China. 2. Department of Histology and Embryology, Bin Zhou Medical College, Yan Tai, P.R. China.
Abstract
BACKGROUND/AIM: The aim of this study was to investigate whether a hydrogen administration can produce neuroprotective effects after brain ischemia reperfusion in rats. MATERIALS AND METHODS: A brain ischemia reperfusion injury was induced by a 2-h left middle cerebral artery occlusion (MCAO) using an intraluminal filament, followed by 46 h of reperfusion. A hydrogen-rich saline (1 mL/kg body weight i.p.) was administered at the beginning of reperfusion. Saline (1 mL/kg)-treated animals were used as the control. Sham-operated animals were also used. Subsequently, 48 h after the MCAO, histological alternations, heme oxygenase-1 (HO-1) expression, and levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in the cerebral cortex and the hippocampus were examined. RESULTS: Hydrogen significantly alleviated brain tissue histological damage, promoted HO-1 expression, upregulated levels of SOD, and decreased the levels of MDA in brain tissue after the ischemia reperfusion injury. CONCLUSION: The results suggest that the neuroprotective effects of hydrogen may be mediated by promoting HO-1 expression and attenuated the oxidative injury.
BACKGROUND/AIM: The aim of this study was to investigate whether a hydrogen administration can produce neuroprotective effects after brain ischemia reperfusion in rats. MATERIALS AND METHODS: A brain ischemia reperfusion injury was induced by a 2-h left middle cerebral artery occlusion (MCAO) using an intraluminal filament, followed by 46 h of reperfusion. A hydrogen-rich saline (1 mL/kg body weight i.p.) was administered at the beginning of reperfusion. Saline (1 mL/kg)-treated animals were used as the control. Sham-operated animals were also used. Subsequently, 48 h after the MCAO, histological alternations, heme oxygenase-1 (HO-1) expression, and levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in the cerebral cortex and the hippocampus were examined. RESULTS:Hydrogen significantly alleviated brain tissue histological damage, promoted HO-1 expression, upregulated levels of SOD, and decreased the levels of MDA in brain tissue after the ischemia reperfusion injury. CONCLUSION: The results suggest that the neuroprotective effects of hydrogen may be mediated by promoting HO-1 expression and attenuated the oxidative injury.