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首页> 外文期刊>Molecular Neurobiology >Protective Effect of Electroacupuncture on Neural Myelin Sheaths is Mediated via Promotion of Oligodendrocyte Proliferation and Inhibition of Oligodendrocyte Death After Compressed Spinal Cord Injury
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Protective Effect of Electroacupuncture on Neural Myelin Sheaths is Mediated via Promotion of Oligodendrocyte Proliferation and Inhibition of Oligodendrocyte Death After Compressed Spinal Cord Injury

机译:通过促进少突胶质细胞增殖和抑制压迫性脊髓损伤后的少突胶质细胞介导电针对神经髓鞘的保护作用。

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Electroacupuncture (EA) has been used worldwide to treat demyelinating diseases, but its therapeutic mechanism is poorly understood. In this study, a custom-designed model of compressed spinal cord injury (CSCI) was used to induce demyelination. Zusanli (ST36) and Taixi (KI3) acupoints of adult rats were stimulated by EA to demonstrate its protective effect. At 14 days after EA, both locomotor skills and ultrastructural features of myelin sheath were significantly improved. Phenotypes of proliferating cells were identified by double immunolabeling of 5-ethynyl-2'-deoxyuridine with antibodies to cell markers: NG2 [oligodendrocyte precursor cell (OPC) marker], 2',3'-cyclic-nucleotide 3'-phosphodiesterase (CNPase) (oligodendrocyte marker), and glial fibrillary acidic protein (GFAP) (astrocyte marker). EA enhanced the proliferation of OPCs and CNPase, as well as the differentiation of OPCs by promoting Olig2 (the basic helix-loop-helix protein) and attenuating Id2 (the inhibitor of DNA binding 2). EA could also improve myelin basic protein (MBP) and protect existing oligodendrocytes from apoptosis by inhibiting caspase-12 (a representative of endoplasmic reticulum stress) and cytochrome c (an apoptotic factor and hallmark of mitochondria). Therefore, our results indicate that the protective effect of EA on neural myelin sheaths is mediated via promotion of oligodendrocyte proliferation and inhibition of oligodendrocyte death after CSCI.
机译:电针(EA)已在世界范围内用于治疗脱髓鞘疾病,但对其治疗机制了解甚少。在这项研究中,使用定制设计的压缩脊髓损伤(CSCI)模型来诱导脱髓鞘。 EA刺激成年大鼠足三里穴(ST36)和泰西穴(KI3),证明其具有保护作用。 EA后14天,髓鞘的运动能力和超微结构特征均得到明显改善。通过对细胞标记物:NG2 [少突胶质细胞前体细胞(OPC)标记物],2',3'-环状核苷酸3'-磷酸二酯酶(CNPase)抗体的5-乙炔基-2'-脱氧尿苷进行双重免疫标记,鉴定了增殖细胞的表型。 )(少突胶质细胞标记)和神经胶质纤维酸性蛋白(GFAP)(星形胶质细胞标记)。 EA通过促进Olig2(基本的螺旋-环-螺旋蛋白)和减弱Id2(DNA结合抑制剂2)来增强OPC和CNPase的增殖,以及OPC的分化。 EA还可以通过抑制caspase-12(内质网应激的代表)和细胞色素c(凋亡因子和线粒体的标志物)来改善髓鞘碱性蛋白(MBP),并保护现有的少突胶质细胞免于凋亡。因此,我们的结果表明,EA对神经髓鞘的保护作用是通过促进CSCI后少突胶质细胞增殖和抑制少突胶质细胞死亡而介导的。

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