目的研究电刺激小脑顶核诱导脑缺血大鼠miRNAs的差异表达谱,筛选与凋亡相关的miRNAs,探讨miRNAs调控电刺激小脑顶核诱导内源性抗凋亡的可能机制。方法将Sprague Dawley大鼠采用随机数字表法分为单纯造模组和预电刺激组(即电刺激小脑顶核1h,24h后制作右侧局灶性脑缺血模型);两组均缺血2h后再灌注,并按再灌注时间不同分为3h,6h、12h、24h、72h亚型(各10只)。通过微阵列芯片分析表达结果。结果电刺激小脑顶核后miR-29c、miR494等表达水平下调,其中miR-29c差异最大,降低了近3倍(P〈0.05)。同时通过生物信息学分析这些表达差异的miRNAs的靶基因,发现了几个凋亡基因相关的miRNAs,如miR-29c。结论电刺激小脑顶核可以诱导脑缺血再灌注大鼠miRNAs表达差异,一些差异表达的miRNAs与凋亡相关。
Objective To detect the difference of these microRNA expression profiles by cerebellar fastigial nucleus electrical stimulation (FNS) in rats with cerebral ischemia and screening miRNAs relative to apoptosis. To explore the endogenous anti-apoptotic mechanism of miRNAs induced by FNS. Methods Sprague-Dawley ( SD ) rats were randomly divided into a vehicle group and a FNS group( electrical stimulation of the FN for 1 h,24 h post-production on the right side of focal eerebralischemia model) , each group was reperfusion of ischemic 2 h and divided 3 h,6 h, 12 h,24 h and 72 h subtypes by different reperfusion ( each 10). The expression was analysed through microarray analysis. Results The expression level of miR-29c and miR-494 down-regulated after electrical stimulation of cerebellar fastigial nucleus, miR-29c has the largest difference, which reduced nearly 3-fold ( P 〈 0.05 ). The bioinformatics analysis indicates that the target genes for these microRNAs were involved in the apoptosis, such as miR-29c. Conclusions MicroRNA expression profiles get more vary following FNS in rats with cerebral isehemia/reperfusion. These microRNAs may associate with apoptosis.