目的 探讨咪唑啉Ⅱ类受体(I2R)高选择性配体2-(2-苯并呋喃基)-2-咪唑啉(2-BFI)对实验性自身免疫性脑脊髓炎(EAE)小鼠脊髓胶质纤维酸性蛋白(GFAP)表达的影响.方法 C57BL/6小鼠30只,随机分成EAE组、2-BFI组和对照组,每组10只.EAE组及2-BFI组给予皮下注射抗原液诱导为EAE模型；2-BFI组同日起腹腔注射2-BFI共14d.各组每日进行2次神经功能缺损评分；第19d进行脊髓病理学检查,免疫组化法观察脊髓炎症细胞浸润、髓鞘脱失程度及GFAP表达.结果 2-BFI组神经功能缺损评分(4.17 ±3.65)明显低于EAE组(10.41±3.02)(P＜0 01)；脊髓病理评分(1.10±0.59)较EAE组(2.38±0.86)显著减少(P＜0.01)；GFAP阳性细胞数[(18.83 ±2.31)个/HP]明显多于EAE组[(12.25 ±2.66)个/HP](P＜0.05).结论 2-BFI能减缓小鼠EAE疾病发展,可能与促进中枢神经系统中GFAP的表达有关.%Objective To investigate the effect of imidazole Ⅱ class receptor (I2R) high selectivity ligands 2-(2-benzofuranyl)-2-imidazoline (2-BF1) on the expression of glial fibrillary acidic portein (GFAP) in spinal cord of mice with experimental autoimmune encephalomyelitis (EAE)- Methods Thirty C57BL/6 mice were divided into EAE group, 2-BF1 group and control group, 10 mice in each group. The EAE and 2-BF1 groups were inducted to be EAE models by subcutaneous injected antigen. And 2-BFI was intraperitoneally injected in 2-BF1 group at same day for 14 d. Then, the score of neurologic impairment was meaeured twice in each group everyday. At 19 d after the modle made, the pathological changes of spinal cord was examinated. The degrees of spinal cord inflammatory cells infiltration and myelin depigmentalion and GFAP expression were observed by immunohistochemislry method. Results The score of neurologic impairment in 2-BFJ group (4. 17 ± 3. 65) was significant lower than EAE group (10. 41 ± 3.02) (P < 0. 01 ) ; the spinal cord pathological score ( 1. 10 ± 0. 59) was significant decreased than EAE group (2.38±0.86)(P<0.01);thequantity of GFAP positive cells [(18.83 ± 2. 31 )/HP] was significantly more than EAE group[(12.25 ±2.66)/HP ](P<0.01) . Conclusion 2-BFI can redunce the EAE development, which maybe related to pormote GFAP expression in central nervous system.
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