论文部分内容阅读
目的:探讨Rho激酶抑制剂法舒地尔(fasudil)联合骨髓源神经干细胞(bone marrow-derived neural stem cells,BM-NSCs)对实验性自身免疫性脑脊髓炎(experimental autoimmune encephalomyelitis,EAE)小鼠的神经保护作用。方法:32只雌性C57BL/6小鼠(8～10周龄),用髓鞘少突胶质细胞糖蛋白35-55(MOG_(35-55))免疫,制备EAE,随机分为对照(ddH_2O)组、fasudil组、BM-NSCs组和fasudil+BM-NSCs组,并分别给予相应处理。免疫后检测小鼠临床症状和相关神经营养因子的表达,Image-Pro Plus 6.0软件进行阳性细胞计数,CraphPad Prism 5软件统计分析。结果:与ddH_2O组比较,fasudil+BM-NSCs处理组明显延迟小鼠的平均起病时间,降低最高临床评分,并缓解EAE小鼠的临床症状;fasudil组、BM-NSCs组和fasudil+BM-NSCs组中脑源性神经营养因子、胶质细胞源性神经营养因子、神经生长因子、神经营养因子3和睫状神经营养因子阳性细胞数均有不同程度的增加,其中,fasudil+BM-NSCs组上述神经营养因子的表达明显多于ddH_2O组、fasudil组和BM-NSCs组(P<0.01)。结论:Fasudil联合BM-NSCs通过协同和叠加效应促进神经营养因子表达,改善中枢神经系统微环境,发挥神经保护作用,从而缓解EAE的临床症状。
Objective: To investigate the effect of Rho kinase inhibitor fasudil combined with bone marrow-derived neural stem cells (BM-NSCs) on experimental autoimmune encephalomyelitis (EAE) mice The neuroprotective effect. Methods: Thirty-two female C57BL / 6 mice (8-10 weeks old) were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG 35-55) to prepare EAE and were randomly divided into control (ddH 2 O ) Fasudil group, BM-NSCs group and fasudil + BM-NSCs group were given corresponding treatment. After immunization, the clinical symptoms and related neurotrophic factor expression in mice were detected. The positive cell counts and the CraphPad Prism 5 software were analyzed by Image-Pro Plus 6.0 software. Results: Compared with the ddH_2O group, the fasudil + BM-NSCs treatment group significantly delayed the average onset time of mice, reduced the highest clinical score and relieved the clinical symptoms of EAE mice. The fasudil, BM-NSCs and fasudil + BM- In NSCs group, the number of brain-derived neurotrophic factor, glial cell line-derived neurotrophic factor, nerve growth factor, neurotrophic factor 3 and ciliary neurotrophic factor positive cells increased in varying degrees, among which fasudil + BM-NSCs Group of neurotrophic factor expression was significantly more than ddH_2O group, fasudil group and BM-NSCs group (P <0.01). CONCLUSIONS: Fasudil combined with BM-NSCs can promote the neurotrophic factor expression through the synergistic and additive effects, improve the central nervous system microenvironment, and exert neuroprotective effects, thereby alleviating the clinical symptoms of EAE.