CAJ | 학술논문

目的：比较不同剂量髓鞘少突胶质细胞糖蛋白35-55(myelin oligodendrocyte glycoprotein 35-55,MOG35-55)多肽片段免疫诱导 C57BL/6小鼠实验性变态反应性脑脊髓炎(experimental autoimmune encephalomyelitis,EAE)其磷酸化酪氨酸蛋白激酶1(phospho-Janus kinase 1,p-JAK1),脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)表达的变化。方法将 C57BL/6小鼠采用数字表法随机分为对照组、MOG35-5550μg(MOG-50)组和 MOG35-55200μg(MOG-200)组。 EAE 小鼠分别以每只动物50μg 或200μg MOG35-55的抗原皮下多点注射诱导造模,对照组乳剂中不含 MOG35-55。观察各组小鼠的发病率、病死率、体质量、神经功能评分的变化。并用 Western blotting 法检测酪氨酸蛋白激酶1(Janus kinase 1,JAK1)及 p-JAK1在皮质中的表达情况；免疫组织化学染色的方法检测 BDNF 在皮质中的表达情况。结果 MOG35-5550μg 和200μg 均能成功诱导 EAE 模型,并增强 p-JAK1的表达,减少 BDNF 的表达。其中 MOG-200组在体质量减轻、神经功能评分及 p-JAK1表达方面较 MOG-50组作用明显,且与对照组相比差异有统计学意义(P<0.05)。结论 MOG-200组 p-JAK1、BDNF 变化明显,可以作为研究药物干预作用的理想模型。
목적：비교불동제량수초소돌효질세포당단백35-55(myelin oligodendrocyte glycoprotein 35-55,MOG35-55)다태편단면역유도 C57BL/6소서실험성변태반응성뇌척수염(experimental autoimmune encephalomyelitis,EAE)기린산화락안산단백격매1(phospho-Janus kinase 1,p-JAK1),뇌원성신경영양인자(brain-derived neurotrophic factor,BDNF)표체적변화。방법장 C57BL/6소서채용수자표법수궤분위대조조、MOG35-5550μg(MOG-50)조화 MOG35-55200μg(MOG-200)조。 EAE 소서분별이매지동물50μg 혹200μg MOG35-55적항원피하다점주사유도조모,대조조유제중불함 MOG35-55。관찰각조소서적발병솔、병사솔、체질량、신경공능평분적변화。병용 Western blotting 법검측락안산단백격매1(Janus kinase 1,JAK1)급 p-JAK1재피질중적표체정황；면역조직화학염색적방법검측 BDNF 재피질중적표체정황。결과 MOG35-5550μg 화200μg 균능성공유도 EAE 모형,병증강 p-JAK1적표체,감소 BDNF 적표체。기중 MOG-200조재체질량감경、신경공능평분급 p-JAK1표체방면교 MOG-50조작용명현,차여대조조상비차이유통계학의의(P<0.05)。결론 MOG-200조 p-JAK1、BDNF 변화명현,가이작위연구약물간예작용적이상모형。
Objective To compare the expressions of phospho-Janus kinase 1(p-JAK1)and brain-derived neurotrophic factor(BDNF) of experimental autoimmune encephalomyelitis(EAE) in C57BL/ 6 mice models induced by myelin oligodendrocyte glycoprotein 35-55 (MOG35-55 ) at different dosages. Methods Thirty female SPF-grade C57BL/ 6 mice with 18-22 gram body weight were divided randomly into three groups: control group and EAE model groups(MOG35-55 50 μg dosage group and MOG35-55 200 μg dosage group). The mice of the two model groups were injected subcutaneously over flanks with the antigen containing 50 μg, 200 μg MOG35-55 / mouse and complete Freund's andjuvant(CFA) in the same volume, respectively. The mice of the control group were injected in the same way phosphate buffered saline(PBS) without containing MOG35-55; 500 ng pertussis toxin(PTX) in 0. 2 mL phosphate buffer solution(PBS) was given by intraperitoneal injection to the mice of the two model groups at 0 and 48 h post-immunization. The mice in control group were injected with PBS in the same way. The disease incidence, death rate, body weight and neurological score of the mice were observed. Meanwhile, the expression of JAK1 and p-JAK1 in cortex were examined by western blotting and brain-derived neurotrophic factor(BDNF) evaluated by immunohistochemical staining. Results The C57BL/ 6 mouse model of EAE was successfully induced by two different dosages of MOG35-55 . The expression of p-JAK1 in cortex were increased while BDNF decreased. However, the influence of MOG35-55 200 μg dosage group on loss of weight, neurological score and the expression of p-JAK1 seemed to be more significant than MOG35-55 50 μg dosage group. Conclusion The mouse model of immune-induced EAE was successfully established with MOG35-55 200 μg and this EAE mouse model is stable and can be used in the drug research of multiple sclerosis(MS).