首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Insulin-like growth factor I treatment reduces demyelination and up-regulates gene expression of myelin-related proteins in experimental autoimmune encephalomyelitis.
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Insulin-like growth factor I treatment reduces demyelination and up-regulates gene expression of myelin-related proteins in experimental autoimmune encephalomyelitis.

机译:在实验性自身免疫性脑脊髓炎中,胰岛素样生长因子I治疗可减少脱髓鞘作用并上调髓鞘相关蛋白的基因表达。

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To compare effects of insulin-like growth factor I (IGF-I) and placebo treatment on lesions that resemble those seen during active demyelination in multiple sclerosis, we induced experimental autoimmune encephalomyelitis in Lewis rats with an emulsion containing guinea pig spinal cord and Freund's adjuvant. On day 12-13, pairs of rats with the same degree of weakness were given either IGF-I or placebo intravenously twice daily for 8 days. After 8 days of placebo or IGF-I (200 micrograms/day or 1 mg/day) treatment, the spinal cord lesions were studied by in situ hybridization and with immunocytochemical and morphological methods. IGF-I produced significant reductions in numbers and areas of demyelinating lesions. These lesions contained axons surrounded by regenerating myelin segments instead of demyelinated axons seen in the placebo-treated rats. Relative mRNA levels for myelin basic protein, proteolipid protein (PLP), and 2',3'-cyclic nucleotide 3'-phosphodiesterase in lesions of IGF-I-treated rats were significantly higher than they were in placebo-treated rats. PLP mRNA-containing oligodendroglia also were more numerous and relative PLP mRNA levels per oligodendrocyte were higher in lesions of IGF-I-treated rats. Finally, a significantly higher proportion of proliferating cells were oligodendroglia-like cells in lesions of IGF-I-treated rats. We think that IGF-I effects on oligodendrocytes, myelin protein synthesis, and myelin regeneration reduced lesion severity and promoted clinical recovery in this experimental autoimmune encephalomyelitis model. These IGF-I actions may also benefit patients with multiple sclerosis.
机译:为了比较胰岛素样生长因子I(IGF-I)和安慰剂治疗对类似于多发性硬化中主动脱髓鞘的病变的影响,我们用含豚鼠脊髓和弗氏佐剂的乳剂诱导了Lewis大鼠实验性自身免疫性脑脊髓炎。在第12-13天,每天两次对具有相同弱点程度的大鼠静脉注射IGF-1或安慰剂,共8天。安慰剂或IGF-I(200微克/天或1毫克/天)治疗8天后,通过原位杂交以及免疫细胞化学和形态学方法研究了脊髓损伤。 IGF-1使脱髓鞘病变的数量和面积显着减少。这些损伤包含被再生髓鞘区段包围的轴突,而不是在用安慰剂治疗的大鼠中看到的脱髓鞘轴突。在IGF-I治疗的大鼠中,髓鞘碱性蛋白,蛋白脂质蛋白(PLP)和2',3'-环核苷酸3'-磷酸二酯酶的相对mRNA水平显着高于安慰剂治疗的大鼠。在IGF-I治疗的大鼠的病变中,含PLP mRNA的少突胶质细胞也很多,每个少突胶质细胞的相对PLP mRNA水平较高。最后,在IGF-I治疗的大鼠的病变中,显着更高比例的增生细胞是少突胶质细胞。我们认为,在这种实验性自身免疫性脑脊髓炎模型中,IGF-I对少突胶质细胞,髓鞘蛋白合成和髓鞘再生的作用降低了病变的严重程度并促进了临床恢复。这些IGF-I作用也可能使多发性硬化症患者受益。

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