少突胶质细胞前体细胞在双环己酮草酰二腙诱导的脱髓鞘模型中的变化特点

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目的观察神经胶质细胞在双环己酮草酰二腙(cuprizone,CPZ)诱导的脱髓鞘模型中的变化特点,探讨其与髓鞘再生的内在联系。方法选8周龄C57BL/6雄性小鼠,分为正常组、急性脱髓鞘组及髓鞘再生组。正常组每天饲养正常鼠粮;模型组小鼠饲养含有0.2%CPZ的混合鼠粮,连续饲养6周;髓鞘再生组在连续喂养6周CPZ鼠粮后,换用正常鼠粮2周。实验过程中通过卢卡斯快蓝染色及透射电镜技术判断脑组织胼胝体区髓鞘脱失及恢复程度,通过免疫组化及免疫荧光技术检测脑内NG2,Olig2和GFAP的表达来评估少突胶质细胞前体细胞及星形胶质细胞的变化特点。结果与正常组相比,急性脱髓鞘组胼胝体髓鞘脱失明显,Olig2、GFAP表达明显升高(P<0.05),侧脑室旁外侧隔核(LSD)NG2升高水平较胼胝体区(CC)更为明显(P<0.05,P<0.01);髓鞘再生组髓鞘有所修复,Olig2、GFAP表达仍高于正常组,但较急性脱髓鞘组有一定程度降低(P<0.05)。结论髓鞘损伤期少突胶质细胞前体细胞不能有效迁移至受损部位,修复期Olig2表达降低,星形胶质细胞持续高水平表达可能是髓鞘修复障碍的影响因素。 Objective To observe the changes of glial cells in demyelinating model induced by cuprizone (CPZ), and to explore its intrinsic relationship with remyelination. Methods Eight-week old C57BL / 6 male mice were divided into normal group, acute demyelination group and remyelination group. The normal mice were fed with normal rat diet every day. The model mice were fed with mixed rat diet containing 0.2% CPZ for 6 weeks. The mice in the remyelination group were fed with normal diet for 2 weeks after 6 weeks of continuous CPZ mice feeding. During the experiment, the rate of demyelination and recovery of myelin in the corpus callosum area was determined by fast blue staining and transmission electron microscopy. The expression of NG2, Olig2 and GFAP in the brain was detected by immunohistochemistry and immunofluorescence assay Characteristics of the changes of the somatic cells and astrocytes in. Results Compared with the normal group, the demyelination of the corpus callosum significantly decreased the expression of Olig2 and GFAP in acute demyelination group (P <0.05), while the level of NG2 in the lateral ventricle lateral septum (LSD) was significantly higher than that in the corpus callosum area (P <0.05, P <0.01). The remyelination of myelin sheath was repaired and the expression of Olig2 and GFAP was still higher than that of normal group, but lower than that of acute demyelination group (P <0.05) . Conclusion The oligodendrocyte precursors can not effectively migrate to damaged sites during myelin sheath injury. The expression of Olig2 is reduced in the repair phase. The sustained high level expression of astrocytes may be the influencing factor of myelin sheath repair.
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