The Effect Of HBO On Expression Of RhoA And MEP In A Rat Focal Cerebral Ischemic Model

Objective: Neurite outgrowth inhibitory protein Nogo-A, MAG and OMGP binds with the Ng-R receptor to activate RhoA intracellular signals and inhibit the plasticity after CNS injury. Hyperbaric oxygen therapy (HBO) has promise as a treatment for acute stroke. We evaluated the effect of HBO on the expression of RhoA and motor evoked potential(MEP) after transient focal cerebral ischemia in a rat with middle cerebral artery occlusion. Methods: Along with the application of intra-luminal technology of Koizumi or Longa, fishing-line (0.23mm in diameter) were used to create the focal cerebral ischemia reperfusion model in health Sprague-Dawley rat, extract the line after occlusion 2h. The successful MCAO rat were divided into therapy group and control group. We estimate the markers as the expression intensity of RhoA protein, nissl body, the pathology and ultra-structure of cerebral ischemical tissue, nerve function scale, amplitude and delitescence of MEP at diffirent time(6h, 12h, 24h, 48h, 96h, 7d and 14d) after MCAO and compare the markers between therapy group and control group. Results:(1)The slight expression of RhoA protein were observed in the cytoplasm in normal brain tissue.(2)Immunohistochemistry showed increased RhoA and RhoA located in the in cytoplasm of the glia cell and nerve cell in cortical and basal ganglia and hippocamp of ischemic area after cerebral ischemia reperfusion, and reached the peak at 48h, decreased after then. The expression were still higher than normal tissue at 7d to 14d.(3)HBO significantly inhibited the expression of RhoA in brain after cerebral ischemia reperfusion(.4)HBO lighten the damage of in pathology and ultrastructure of brain tissue after cerebral ischemia reperfusion.(5)HBO improved the amplitude and delitescence of MEP in the rats after cerebral ischemia reperfusion. Conclusion: (1)The enhanced expression of RhoA in the acute cerebral ischemia phase and recovery phase suggested that the endogenic mechanism activated by cerebral ischemic injury had inhibited neurological function rehabilitation. (2)HBO could reduce the pathological damages of brain tissue, and also increase rat's neurological function scale , and improve MEP, that showed a neuroprotective effect in acute stage and rehabilitation effect in recovery phase. (3)HBO could reduce the over expression of RhoA protein at every time checkpoints after cerebral ischemia. The effect was parallel with the change of MEP and neurological function scale, suggested that the rehabilitation effect of HBO treatmentpartially corresponded to regulating RhoA signal pathway.