| Objective: To investigate the regulatory mechanisms of miR-29c in focalcerebral ischemia reperfusion injury of rats with Pre-stimulation of cerebellarfastigial nucleus.Methods: Spragu-Dawley (SD) rats were randomly divided into3groups：sham operation group,modeling group and Fastigial nucleus electricalstimulation(FNS) group. Each groups were reperfusion24h of ischemic2h. TTCstaining was employed to measure ischemic lesion volumes ration;theexpression of miR-29c and BIRC2mRNA level was detected by real-timeqPCR;Western blotting was used to observe BIRC2protein expressions;Theapoptotic cells were detected by TUNEL assay; Build BIRC2luciferase reportergene vectors, luciferase reporter gene detection system detect the expression ofluciferase.Results:(1) Infarct volume measurement results: FNS group comparedwith modeling group: Infarct volume ratio reduced of30.20%(p<0.01);(2) PCRresults: Sham group、FNS group、modeling group：The relative expression of miR-29c（1.0、0.343±0.009、0.955±0.212），FNS group compared with modelinggroup，the expression of miR-29c drops to approximately3times(p<0.01); Therelative expression of BIRC2（1.0、2.404±0.330、1.168±0.247），FNS groupcompared with modeling group，the expression of BIRC2mRNA increased morethan2times(p<0.01);（3）BIRC2protein expression test results：Sham group、FNS group、modeling group（0.5±0.364、1.407±0.270、0.939±0.227），BIRC2protein expression was increased1.5-fold(p<0.05);（4） TUNEL apoptosisdetection results：the number of apoptotic cells of FNS group（22.37±1.27）compared with the number of apoptotic cells of modeling group（35.9±1.93），apoptotic cells decreased37.68%(p<0.01);（5） Dual luciferase reportgene system shows that miR-29c can inhibit the expression of reportergene containing the BIRC23’UTR wild type recognition element(p<0.01).Conclusion: Pre-electrical stimulation can decrease the expression ofmiR-29c, miR-29c regulation the focal cerebral ischemia-reperfusion injury byregulating the expression of BIRC2. |
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