BACKGROUND: Due to its antioxidant and anti-inflammatory properties, hydrogen gas (H(2)) has protective effects on a variety of organs from damage induced by ischemia/reperfusion (I/R). In this study, we tested the protective effect of hydrogen-rich saline on the brain in a global cerebral I/R model. MATERIALS AND METHODS: We used a four-vessel occlusion model of global cerebral ischemia (15 min) and reperfusion with rats. The rats were divided into four groups (n = 96): sham, I/R plus physiologic saline injected intraperitoneally, I/R plus hydrogen-rich saline injected intraperitoneally at the beginning of reperfusion, and I/R plus hydrogen-rich saline injected intraperitoneally 6 h after reperfusion began. One group of rats was sacrificed after 24 h of reperfusion. Malondialdehyde (MDA) was measured to quantify the oxidative stress. Caspase-3 was measured to indicate the status of apoptosis. Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and nuclear factor-κB (NF-κB) were measured to monitor the inflammation. Another group of rats was sacrificed after 72 h of reperfusion to measure the histologic damages in hippocampus by hematoxylin and eosin staining and Nissl staining. RESULTS: Compared with rats with I/R only, hydrogen-rich saline treatment significantly improved the amount of surviving cells. NF-κB, TNF-α, IL-6, MDA, and caspase-3 were all increased significantly by I/R injury. Hydrogen-rich saline reduced all these markers. CONCLUSIONS: Our data demonstrate that intraperitoneal injection of hydrogen-rich saline has strong protective effect on the transient global cerebral ischemia-reperfusion rats.
BACKGROUND: Due to its antioxidant and anti-inflammatory properties, hydrogen gas (H(2)) has protective effects on a variety of organs from damage induced by ischemia/reperfusion (I/R). In this study, we tested the protective effect of hydrogen-rich saline on the brain in a global cerebral I/R model. MATERIALS AND METHODS: We used a four-vessel occlusion model of global cerebral ischemia (15 min) and reperfusion with rats. The rats were divided into four groups (n = 96): sham, I/R plus physiologic saline injected intraperitoneally, I/R plus hydrogen-rich saline injected intraperitoneally at the beginning of reperfusion, and I/R plus hydrogen-rich saline injected intraperitoneally 6 h after reperfusion began. One group of rats was sacrificed after 24 h of reperfusion. Malondialdehyde (MDA) was measured to quantify the oxidative stress. Caspase-3 was measured to indicate the status of apoptosis. Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and nuclear factor-κB (NF-κB) were measured to monitor the inflammation. Another group of rats was sacrificed after 72 h of reperfusion to measure the histologic damages in hippocampus by hematoxylin and eosin staining and Nissl staining. RESULTS: Compared with rats with I/R only, hydrogen-rich saline treatment significantly improved the amount of surviving cells. NF-κB, TNF-α, IL-6, MDA, and caspase-3 were all increased significantly by I/R injury. Hydrogen-rich saline reduced all these markers. CONCLUSIONS: Our data demonstrate that intraperitoneal injection of hydrogen-rich saline has strong protective effect on the transient global cerebral ischemia-reperfusion rats.