H2 Fails to Improve Outcomes in Rats After Intracerebral HemorrhageScientific Research
original title: Hydrogen does not Exert Neuroprotective Effects or Improve Functional Outcomes in Rats After Intracerebral HemorrhageDOI: 10.5137/1019-5149.JTN.14098-15.1
Aim: Increasing evidence suggests that reactive oxygen species damage the blood-brain barrier and increase brain edema after intracerebral hemorrhage (ICH). Recently, strong clinical and experimental evidence has shown that hydrogen has potent protective cellular effects in various diseases. However, the effect of hydrogen on ICH remains unclear. The present study investigates whether hydrogen has neuroprotective effects and improves functional outcome in the rat ICH model. Material and methods: ICH model was generated by injecting 50 μl autologous tail artery blood stereotactically into the right caudate nucleus of Sprague-Dawley rats. Rats were randomly divided into four groups: sham, ICH/vehicle, ICH/hydrogen gas, and ICH/hydrogen-rich saline groups. Hydrogen treatment was performed for 3 days. The evaluation of functional outcome was done before, and at 24 and 72 hours after ICH. Hemorrhage volume, immunohistochemistry for 8-hydroxy-2′-deoxyguanosine (8-OHdG), and brain water content were evaluated at 72 hours after ICH.
Results: Hydrogen administration reduced the expression of 8-OHdG in the brain, but did not attenuate brain water content or improve functional outcome, regardless of administration route.
Conclusion: Hydrogen administration without surgery has no neuroprotective effect in the blood injection rat ICH model.