背景：神经生长因子是一种具有神经元营养作用的细胞调节因子，对神经干细胞的增殖具有促进作用。 目的：观察神经生长因子对实验性自身免疫性脑脊髓炎幼年大鼠脑神经干细胞的影响。 方法：将3周龄Wistar幼鼠随机分为对照组、脑脊髓炎模型组、脑脊髓炎神经生长因子治疗组，后2组建立实验性自身免疫性脑脊髓炎幼鼠模型，脑脊髓炎神经生长因子治疗组在发病当天起腹腔注射神经生长因子(1000 U/kg)，共7 d，对照组和模型组幼鼠不予处理。观察神经生长因子对实验性自身免疫性脑脊髓炎幼鼠临床症状的影响，以及各组幼鼠室管膜下区Brdu(神经干细胞标记物)、皮质区Brdu+/GFAP+(星形胶质细胞标记物)的表达变化。 结果与结论：①模型鉴定：实验性自身免疫性脑脊髓炎模型幼鼠在免疫后10 d开始陆续出现脑脊髓炎症状，对照组未出现脑脊髓炎症状；模型组幼鼠脑组织中胶质细胞增生，炎症细胞浸润，血管内皮细胞增生破坏，炎症细胞集中在血管周围；对照组脑组织表现正常；②临床症状：脑脊髓炎神经生长因子治疗组的症状持续时间低于脑脊髓炎模型组(P<0.05)，平均神经功能评分低于脑脊髓炎模型组(P<0.05)；③室管膜下区Brdu的表达：脑脊髓炎模型组幼鼠高于对照组(P<0.05)，发病后7，21 d脑脊髓炎神经生长因子治疗组室管膜下区Brdu的表达显著高于脑脊髓炎模型组(P<0.05)；④皮质区Brdu+/GFAP+表达：脑脊髓炎模型组高于对照组(P<0.05)，发病后7，21 d脑脊髓炎神经生长因子治疗组皮质区Brdu+/GFAP+的表达显著高于脑脊髓炎模型组(P<0.05)；⑤结果表明，自身免疫性脑脊髓炎幼鼠模型被成功建立，神经生长因子治疗能够改善实验性自身免疫性脑脊髓炎幼鼠的临床症状，促进神经干细胞的增殖，并分化为星形胶质细胞。%BACKGROUND:Nerve growth factor is a neurotrophic factor that is involved in the cel regulation and promotes the proliferation of neural stem cel s. OBJECTIVE:To observe the effect of nerve growth factor on neural stem cel s of experimental autoimmune encephalomyelitis rats. METHODS:Wistar rats, 3 weeks of age, were randomly divided into control group, encephalomyelitis model group, nerve growth factor treatment group. Rat models of experimental autoimmune encephalomyelitis were made in the latter two groups. On the day of onset, rats in the nerve growth factor treatment group were given intraperitoneal injection of 1 000 U/kg nerve growth factor for 7 continuous days, and rats in the other two groups given no treatment. Effects of nerve growth factor on clinical symptoms of model rats were observed. Expression of Brdu in the subependymal zone and Brdu+/GFAP+expression in the cortex were detected. RESULTS AND CONCLUSION:Rat models of experimental autoimmune encephalomyelitis appeared to have encephalomyelitis symptoms successively at the beginning of 10-day immunization, while rats in the control group had no symptoms of encephalomyelitis. In the model group, glial cel hyperplasia, inflammatory cel infiltration, damage to vascular endothelial cel proliferation, and perivascular aggregation of inflammatory cel s in the rat brain were found, while no abnormal changes in the rat brain were found in the control group. Compared with the model group, the expression of Brdu in the subependymal zone and Brdu+/GFAP+expression in the cortex were both higher in the model group (P<0.05), and these expressions were also higher in the nerve growth factor treatment group than the model group at 7 and 21 days after onset (P<0.05). To conclude, these findings suggest that the rat model of autoimmune encephalomyelitis can be successful y established, and nerve growth factor treatment can improve clinical symptoms of experimental autoimmune encephalomyelitis rats by promoting the proliferation and differentiation of neural stem cel s into astrocytes.
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