Abstract
Influence of a new antioxidant compound H-290/51 on carbon monoxide (CO) production following spinal cord injury was examined using immunohistochemistry of the constitutive isoform of heme oxygenase-2 (HO-2) in a rat model. Subjection of rats to 5 h spinal cord injury by making an incision into the right dorsal horn of the T10-11 segments resulted in upregulation of HO-2 in the injured and adjacent T9 and T12 segments. At this time, disruption of the blood-spinal cord barrier (BSCB) permeability, edema formation and cell injury were more pronounced. Pretreatment with H-290/51 (50 mg/kg, p.o., 30 min before trauma) significantly attenuated the HO-2 immunoreactivity along with breakdown of the BSCB permeability, edema and cell injury. These results for the first time demonstrate that the antioxidant compound H-290/51 is capable of attenuating HO-2 expression and thereby influencing CO production. Furthermore, our observations indicate that oxidative stress is involved in CO production, as reflected by HO-2 expression, which is injurious to the cord and H-290/51 exerts powerful neuroprotective effects in spinal cord injury.
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