The neuroprotective effect of inhaled hydrogen sulfide against delayed paraplegia after spinal cord ischemia in mice

硫化氢(H_2S)是已知的内源性气体分子之一，具有抗炎、清除自由基、抗细胞凋亡等作用。我们观察了80ppm×5小时吸入H_2S对小鼠脊髓缺血后迟发性截瘫的神经保护作用。我们实验的结果是，吸入硫化氢的小鼠在再灌流72小时后表现出显著改善的神经学结果，同时保留了脊髓腹角正常神经元的数量。此外，与对照组相比，吸入硫化氢显著抑制了脊髓腹角caspase3的表达。提示吸入硫化氢对脊髓缺血后的脊髓腹侧神经元有保护作用，这种保护作用可能与其抗细胞凋亡作用有关。

Hydrogen sulfide (H2S), well-known for one of endogenous gas molecules, is reported to possess potency of anti-inflammation, radical scavenging effect,and anti-apoptotic effect, etc. We have investigate the neuroprotective effect of inhaled H2S (80ppm x 5 hrs) against delayed onset paraplegia after spinal cord ischemia in mice. As a result from our experiments, mice treated with inhaled hydrogen sulfide showed significant better neurological outcome at 72 hrs of reperfusion with preserving the number of normal neurons in spinal ventral horn. Additionally, inhaled H2S suppressed the expression of cleaved caspase3 in the spinal ventral horn significantly comparing with control group. According to the present data, it is suggested that inhaled H2S potentially protect spinal ventral neurons after spinal cord ischemia, and this protective effect might be associated with its anti-apoptotic effect.