论文部分内容阅读
目的:观察小鼠在脊髓损伤(SCI)后,醛糖还原酶(AR)在脊髓损伤后修复过程中的作用及可能的机制。方法:采用C57BL/6-ar+/+(B6野生型小鼠)和C57BL/6-ar-/-(B6-AR基因敲除)小鼠,建立脊髓重度夹伤模型。首先分析了AR分子在损伤脊髓中的细胞表达类型及脊髓损伤后AR分子mRNA的表达水平变化情况;通过BBB运动学分析,比较AR基因敲除小鼠和野生型小鼠脊髓损伤后运动功能恢复情况,对比损伤区面积变化;通过qRT-PCR方法,检测对比M1/M2型巨噬细胞特异分子iNOS和Arg I的表达变化。结果:AR分子在野生型小鼠损伤脊髓中的小胶质/巨噬细胞中高表达;qRT-PCR研究发现:脊髓损伤后AR表达逐渐升高,在损伤后第3天达到高峰。AR敲除小鼠在脊髓损伤后,其运动功能恢复好于野生型小鼠(P<0.05),同时损伤区面积也小于对照组。AR基因缺失后,损伤脊髓中的小胶质/巨噬细胞通过高表达Arg I向M2型巨噬细胞方向极化。结论:AR通过调节脊髓中小胶质/巨噬细胞的极化来影响脊髓损伤后的修复。
AIM: To investigate the role of aldose reductase (AR) in repairing spinal cord injury after spinal cord injury (SCI) in mice and its possible mechanism. Methods: A severe spinal cord injury model was established in C57BL / 6-ar + / + (B6 wild-type mice) and C57BL / 6-ar - / - (B6- AR knockout) mice. Firstly, we analyzed the expression of AR in rat spinal cord injury and AR mRNA expression after spinal cord injury. By BBB kinematics analysis, the motor function of AR knockout mice and wild-type mice were compared after spinal cord injury The changes of lesion area were compared. The expression of iNOS and Arg I in M1 / M2 macrophages were detected by qRT-PCR. Results: AR molecules were highly expressed in microglial / macrophages in the injured spinal cord of wild-type mice. The qRT-PCR results showed that AR expression gradually increased after spinal cord injury and peaked on the 3rd day after injury. After spinal cord injury, AR knockout mice recovered better motor function than wild-type mice (P <0.05), meanwhile, the lesion area was also smaller than that of the control group. After deletion of AR gene, microglial / macrophages in injured spinal cord are polarized towards M2 macrophages through high expression of Arg I. Conclusion: AR affects the repair of spinal cord injury by regulating the polarization of microglia / macrophage in the spinal cord.