抄録
It has recently been reported that hydrogen gas (H2) acts as a radical scavenger by reducing the hydroxyl radical and reduces acute oxidative stress on brain in ischemia-reperfusion stress (Ohsawa et al., Nat. Med. 2007). We measured high-energy phosphates in rat brain slices by phosphorus nuclear magnetic resonance (31P-NMR) and evaluated neuroprotective effects of H2 using a hypoxic stress model and an ischemic-reperfusion model. Brain slices were superfused with well-oxygenated (PO2 ≈ 500Torr) artificial cerebrospinal fluid (ACSF) equilibrated with (H2+ group) or without 4% H2 gas (H2- group) at 300K. In the hypoxic stress model, slices were superfused with hypoxic ACSF (PO2 ≈ 120Torr) for 2 hours. In the ischemia-reperfusion model, perfusion was stopped for 1 hour. In the hypoxic stress model, phosphocreatine (PCr) level of H2+ group recovered to 81% relative to the pre-stress level, whereas that of H2- group was 85% (n.s.). There was no significant difference in γ-ATP levels. In the ischemia-reperfusion model, PCr levels after stress were not significantly different between the two groups (H2+: 38%, H2-: 41%; p > 0.05). But γ-ATP levels of H2+ group 1-2 hours after stress were significantly higher than that of H2- group (H2+: 39%, H2-: 26%; p < 0.05). CONCLUSION: Our result might indicate the neuroprotective effect of H2 gas in an ischemic-reperfusion model from a viewpoint of energy metabolism. [J Physiol Sci. 2008;58 Suppl:S216]
