The Mechanism Of MiR-181c Induced Neuroprotection By Hypoxia Preconditioning In Rats

Objective To study the molecular mechanisms of miR-181c induced neuroprotectionin hypoxia preconditioning and ischemic SD rats, to discuss the effect and molecular ofmiR-181c and mitochondrial oxidative synthase1subunits in ischemic injury.Methods Thirty-nine SD-rats were randomly divided into five groups, control group(n=5), sham-operated group (n=5), the operated of middle cerebral artery occlusion group(MCAO, n=12), hypoxia-preconditioned group(HPC, n=5), hypoxia-preconditioned andmiddle cerebral artery occlusion group (n=12). We assessed the animal models byneurological deficit score, after6hours’ surgery, through measured infarct size and finallyanalyzed with the image software. Quantitative Reverse Transcript-PCR assay was appliedto detect the expression levels of miR-181c and western blotting was used to verify thetarget protein of mt-COX1.Results Under the treatment of hypoxia-preconditioned, the neurological impairmentwas alleviated (p=0.004), and the infarct volume was reduced significantly from22.50±2.96%to16.40±3.13%(p<0.001). The express of miR-181c was down-regualted(0.66-fold, p<0.001), but it showed up-regulation (3.05-fold, p<0.001) significantly afterconduted with MCAO conditionings. The surgical group with pre-treatment was alsoup-regulated (1.89-fold, p<0.001), but which was still down-regulate compare group withonly suffered MCAO. The expressions of protein during those groups were changedsignificantly (F=178.60，p<0.001). The highest expressions of mt-cox1was the surgicalgroup without pre-treatment (0.93±0.04), then followed with the surgical group withpre-treatment, the hypoxia-preconditioned group was also increased.Conclusions Hypoxia preconditioning alleviated the neurological impairment and reduced the infarct volume, which also reduce the damage of neurons. The express ofmiR-181c was down regulated after hypoxia-preconditioned which makes increased theexpressions of mt-cox1, thus enhanced the mitochondrial respiratory function. Thissuggested that miR-181c might involved in the neuroprotection induced by hypoxiaprecondition.