Effects of hydrogen-rich saline given during reperfusion on global cerebral ischemia-reperfusion injury in rats
Kangli Hui, Qing Ji, Manlin Duan
Abstract
Kangli Hui, Qing Ji, Manlin Duan
Abstract
Objective To evaluate the effect of hydrogen-rich saline given during reperfusion on global cerebral ischeraia-reperfusion (I/R) injury in rats.Methods Seventy-two adult male SD rats,aged 2.0-2.5 months,weighing 260-300 g,were randomly divided into 3 groups (n = 24 each):sham operation group (group S),group I/R and hydrogen-rich saline group (group H).In groups I/R and H cerebral I/R was induced by occlusion of 4 vessels( cauterization of bilateral carotid arteries and 15 min occlusion of bilateral common carotid arteries).In group H intraperitoneal 0.6 mmol/L hydrogen-rich saline 5 ml/kg was injected at 6 h of reperfusion,while equal volume of normal saline was injected instead of hydrogen-rich saline.Eighteen rats of each group were sacririced at 24 h of reperfusion,and then the hippocampi were removed for determination of malondialdehyde (MDA),tumor necrosis factor-α (TNF-α),interleukin-6 (IL-6)contents,and nuclear factor-κB (NF-κB) activity and activated caspase-3 expression.Another six rats of each group were sacrificed at 72 h of reperfusion,and then brain tissues were removed for microscopic examination and counting the number of uninjured pyramidal cells in hippocampal CA1 region.Results Compared with S group,the contents of MDA,TNF-α,IL-6 and NF-κB activity were significantly increased,activated caspase-3 expression was significantly up-regulated,uninjured pyramidal cells in hippocampal CA1 region were significantly decreased in I/R group( P < 0.05).Hydrogen-rich saline given during reperfusion attenuated the above-mentioned I/R-induced changes( P < 0.05 ).The histologic damage of the hippocampal CA1 region was significantly slighter in group H than group I/R.Conclusion Hydrogen-rich saline given during reperfusion can reduce global cerebral I/R injury in rats through inhibition of lipid peroxidation,inflammatory response and apoptosis. Key words: Hydrogen; Reperfusion injury; Brain
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Objective To evaluate the effect of hydrogen-rich saline given during reperfusion on global cerebral ischeraia-reperfusion (I/R) injury in rats.Methods Seventy-two adult male SD rats,aged 2.0-2.5 months,weighing 260-300 g,were randomly divided into 3 groups (n = 24 each):sham operation group (group S),group I/R and hydrogen-rich saline group (group H).In groups I/R and H cerebral I/R was induced by occlusion of 4 vessels( cauterization of bilateral carotid arteries and 15 min occlusion of bilateral common carotid arteries).In group H intraperitoneal 0.6 mmol/L hydrogen-rich saline 5 ml/kg was injected at 6 h of reperfusion,while equal volume of normal saline was injected instead of hydrogen-rich saline.Eighteen rats of each group were sacririced at 24 h of reperfusion,and then the hippocampi were removed for determination of malondialdehyde (MDA),tumor necrosis factor-α (TNF-α),interleukin-6 (IL-6)contents,and nuclear factor-κB (NF-κB) activity and activated caspase-3 expression.Another six rats of each group were sacrificed at 72 h of reperfusion,and then brain tissues were removed for microscopic examination and counting the number of uninjured pyramidal cells in hippocampal CA1 region.Results Compared with S group,the contents of MDA,TNF-α,IL-6 and NF-κB activity were significantly increased,activated caspase-3 expression was significantly up-regulated,uninjured pyramidal cells in hippocampal CA1 region were significantly decreased in I/R group( P < 0.05).Hydrogen-rich saline given during reperfusion attenuated the above-mentioned I/R-induced changes( P < 0.05 ).The histologic damage of the hippocampal CA1 region was significantly slighter in group H than group I/R.Conclusion Hydrogen-rich saline given during reperfusion can reduce global cerebral I/R injury in rats through inhibition of lipid peroxidation,inflammatory response and apoptosis. Key words: Hydrogen; Reperfusion injury; Brain
Key concepts: Saline, Malondialdehyde, Reperfusion injury, Hippocampal formation, Anesthesia, Intraperitoneal injection, Endocrinology, Ischemia