摘要
目的探讨骨髓间充质干细胞(BMSC)对损伤的脊髓神经元存活及神经突生长的影响。方法利用脊髓损伤部位组织提取液处理神经元,建立细胞损伤模型。将BMSC与损伤神经元共培养,通过免疫细胞化学染色、MTT等实验手段检测神经元的存活及神经突的生长情况。为了确定BMSC是否通过分泌SDF-1发挥作用,我们应用RNAi技术沉默BMSC中SDF-1基因的表达,进一步选用SDF-1受体CXCR4、CXCR7的阻断剂AMD3100和CCX771,再次检测各组中神经元的存活及神经突的生长情况,探讨SDF-1可能的作用途径。结果与损伤神经元单独培养组相比,BMSC和损伤神经元共培养组中,神经元存活的数量提高,神经突的长度增长,差异显著(P<0.05)。shS DF-1 BMSC和损伤神经元共培养组中,神经元存活数量、神经突的长度也有所增加,但无显著性差异(P>0.05)。同时,CXCR4受体阻断剂抑制了BMSC对神经元的保护作用及对神经突生长的促进作用,而CXCR7受体阻断剂的影响不明显。结论 BMSC分泌SDF-1促进损伤神经元的存活及神经突的生长,该作用可能通过CXCR4受体途径实现。
Objective To study the effects of bone marrow mesenchymal stem cells （BMSCs） on survival and neurites outgrowth of neurons in spinal cord injury mice. Methods The neuron injury model was made by treatment with tissue extracts from injured spinal cord. The survival and neurites outgrowth of injured neurons were determined by immunocytochemistry and MTT in the co-cultured injured neurons and BMSCs, and in stromal-derived factor 1 （SDF-1） silenced group, and in SDF-1 receptors CXCR4 antagonist （AMD3100） and CXCR7 antagonist （CCX771） groups. Results Compared with control group, BMSCs increased survival and neurites outgrowth of injured neurons（P〈0.05）, however, CXCR4 antagonist （AMD3100） inhibited the effect of BMSCs, but not for CXCR7 antagonist （CCX771）. shSDF-1 BMSCs promoted survival and neurites outgrowth of injured neurons, but without significant differences （P〉0.05） . Conclusion The promotion effect of BMSCs on survival and neurites outgrowth of injured neurons might be related to the secretion of SDF-1 via CXCR4 receptor.
出处
《解剖科学进展》
2016年第6期640-645,649,共7页
Progress of Anatomical Sciences
基金
黑龙江省教育厅科学技术研究项目基金(12541477)
