UNASSIGNED: C57BL/6J mice were subjected to SCIR by crossclamping the aortic arch and left subclavian artery for 5.5 minutes. Two hours after reperfusion, hBM-MSCs (hBM-MSC group) or phosphate-buffered saline (control group) were intravenously injected without immunosuppressant. Hindlimb motor function was assessed until day 28 after reperfusion using the Basso Mouse Scale (BMS). The lumbar spinal cord was harvested at hour 24 and day 28, and the histologic number of NeuN-positive motor neurons in 3 cross-sections of each lumbar spinal cord and the gene expression were evaluated.
UNASSIGNED: BMS score was 0 throughout the study period in all control mice. BMS score was significantly greater in the hBM-MSC group than the control group from hour 8 (P < .05) to day 28 (P < .01). The numbers of motor neurons at hour 24 (P < .01) and day 28 (P < .05) were significantly preserved in the hBM-MSC group than the control group. mRNA expression levels of proinflammatory cytokines were significantly lower (P < .05), and those of insulin-like growth factor-1 (P < .01) and proangiogenic factors (P < .05) were significantly greater in the hBM-MSC group than the control group at hour 24.
UNASSIGNED: hBM-MSC therapy may attenuate SCIR injury by preserving motor neurons, at least in part, through inhibition of proinflammatory cytokines and upregulation of proangiogenic factors in the reperfusion-injured spinal cord.
UNASSIGNED:C57BL/6J小鼠通过交叉夹持主动脉弓和左锁骨下动脉5.5分钟进行SCIR。再灌注后两小时,静脉内注射hBM-MSC(hBM-MSC组)或磷酸盐缓冲盐水(对照组),不使用免疫抑制剂。使用Basso小鼠量表(BMS)评估后肢运动功能直至再灌注后第28天。在第24小时和第28天收获腰脊髓,并评估每个腰脊髓3个横截面中NeuN阳性运动神经元的组织学数量和基因表达。
UNASSIGNED:在所有对照小鼠的整个研究期间,BMS评分为0。从第8小时(P<0.05)到第28天(P<0.01),hBM-MSC组的BMS评分明显高于对照组。hBM-MSC组在第24小时(P<0.01)和第28天(P<0.05)的运动神经元数量明显高于对照组。促炎细胞因子mRNA表达水平显著降低(P<0.05),hBM-MSC组在24小时的胰岛素样生长因子-1(P<.01)和促血管生成因子(P<.05)明显高于对照组。
未经证实:hBM-MSC治疗可能通过保留运动神经元来减轻SCIR损伤,至少在某种程度上,通过抑制促炎细胞因子和上调再灌注损伤脊髓中的促血管生成因子。