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目的探讨微小RNA-181b(miR-181b)在缺血性脑卒中小鼠脑损伤中的作用及机制。方法采用小鼠大脑中动脉阻塞(MCAO)模型模拟缺血性脑损伤;Real-time PCR检测miR-181b mRNA表达情况;蛋白印迹观察miR-181b靶蛋白热休克蛋白A5(HSP A5)蛋白水平变化情况;Nissl方法检测皮层缺血神经元的缺失情况;行为学方法评估小鼠的神经行为学功能损伤程度。结果侧脑室注射miR-181b拮抗剂可使脑内miR-181b表达水平明显降低(P<0.05,n=3);MCAO后小鼠的神经行为学功能受到严重损伤,miR-181b拮抗剂可明显缓解这些行为学改变(P<0.05,n=6);下调miR-181b可以提高HSPA5蛋白水平(P<0.05,n=3);MCAO后小鼠皮层有一定程度的神经细胞缺失,预先给予miR-181b拮抗剂发挥保护作用,神经细胞缺失减少(P<0.05,n=3)。结论 miR-181b可能通过调节HSPA5蛋白的表达在缺血性脑卒中小鼠脑损伤中发挥重要作用。
Objective To investigate the effect and mechanism of microRNA-181b (miR-181b) on brain injury in mice with ischemic stroke. Methods The middle cerebral artery occlusion (MCAO) model of mice was used to simulate ischemic brain injury. The expression of miR-181b mRNA was detected by Real-time PCR. The protein level of miR-181b target protein was detected by Western blotting. Nissl method to detect the absence of cortical ischemic neurons; behavioral methods to assess the degree of neurobehavioral impairment in mice. Results The intracerebroventricular injection of miR-181b antagonist significantly reduced the expression of miR-181b in brain (P <0.05, n = 3). The neurobehavioral function of MCAO mice was severely damaged and the antagonist of miR-181b (P <0.05, n = 6); downregulation of miR-181b can increase the HSPA5 protein level (P <0.05, n = 3); after MCAO mouse cortex has a certain degree of nerve cell loss, pre-miR -181b antagonist exerted a protective effect and decreased neuronal loss (P <0.05, n = 3). Conclusion miR-181b may play an important role in the brain injury induced by ischemic stroke in mice by regulating the expression of HSPA5 protein.