The Mechanism Of TRPC3 In Ischemic Brain Injury After Hypoxia Preconditioning In Rats

Objective To study wether TRPC3 has neuroprotection and its molecular mechanisms in hypoxia preconditioning SD rats, to discuss the effect and molecular mechanisms of TRPC3 and e NOS in ischemic brain injury.Methods Randomly divede ninety two SD-rats into seven groups: control group(N, n=13), sham-operated group(S, n=13), the operated of middle cerebral artery occlusion group(M, n=14), hypoxia-preconditioned group(HP, n=14), hypoxia-preconditioned and middle cerebral artery occlusion group(M, n=14), intracerebroventricular injection control and middle cerebral artery occlusion group(IC, n=13), inhibitor intracerebroventricular injection control and middle cerebral artery occlusion group(ICP, n=13).Animal models after 24 hours’ surgery were assessed by neurological deficit score through infarct size, then analyze with the Image J.Expression levels of TRPC3 and e NOS were detected by RT-PCR, and immunohistochemical was used to verify the target protein of TRPC3 and e NOS.Results The impairment was alleviated after hypoxia-preconditione, and the infract volume was reduced significantly(P<0.01).Compared to IC, the infract volume of ICP was increased significantly(P<0.05).Compared with N, expression of TRPC3 and e NOS in HP was up-regulated(P<0.01), expression of TRPC3 in M was down-regulated( P < 0.01), and expression of TRPC3 in HM was also down-regulated(P<0.05), but the reducment in M was significantly(P<0.05). Immunohistochemical results: Compared with N, expression of TRPC3 and e NOS in HP was up-regulated(P<0.01); Compared with M, expression of TRPC3 and e NOS in HM was up-regulated(P<0.01); Compared to ICP, expression of TRPC3 and e NOS in IC was up-regulated(P<0.05).Conclusions Hpoxia preconditioning improved the neurological impairment, reduced the volume, and protected neurons from damage.TRPC3 and e NOS might involve in the neuroprotection induced by hypoxia precondition.Hypoxia precondition might reduce ischemic brain injury via increase the expression of TRPC3 and e NOS.