P39 Inhaled hydrogen sulfide can prevent delayed neuronal death after spinal cord ischemia in mice

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• 作者：Manabu Kakinohana^a ; Kotaro Kida^b ; Fumito Ichinose^b
• 刊名：Nitric Oxide
• 出版年：30 May 2014
• 年：2014
• 卷：39
• 期：supp_S
• 页码：S28
• 全文大小：39 K

文摘

Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H₂S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5 min. Mice breath air alone (Control) or air mixed with H₂S (80 ppm) for 5 h (H₂S group), starting at 23 h after 5 min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72 h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5 min SCI showed mild and transient motor dysfunction at 24 h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48 h of reperfusion. In contrast, six of nine mice in H₂S goup did not show any developments of neurological dysfunction from 48 h after 5 min SCI. 5 min SCI did not affect gene expression of IL-6 or TNFalpha at 8 h of reperfusion. Whereas those gene expression in control group increased starting at 30 h after reperfusion and significantly higher at 48 h than preischemia, inahled H₂S (H₂S group) significantly suppressed gene expression of inflammatory cytokine at 48 h after ischemia compared with Control group. According to our data, inhaled H₂S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects.