上海医学
上海醫學
상해의학
SHANGHAI MEDICAL JOURNAL
2010年
1期
78-80,封3
,共4页
多发性硬化%实验性自身免疫性脑脊髓膜炎%干预%α-硫辛酸
多髮性硬化%實驗性自身免疫性腦脊髓膜炎%榦預%α-硫辛痠
다발성경화%실험성자신면역성뇌척수막염%간예%α-류신산
Experimental autoimmune encephalomyelitis%Multiple sclerosis%Interference%α-lipoic acid
目的 研究α-硫辛酸(α-LA)对实验性自身免疫性脑脊髓炎(EAE)大鼠模型干预的有效性,探讨α-LA临床治疗多发性硬化的可能性.方法 Wistar大鼠30只,其中22只制作EAE模型,分为α-LA干预组(11只)及免疫组(11只),另8只为非免疫组.α-LA干预组大鼠于免疫当天开始每天1次腹腔注射α-LA(100 mg/kg),至实验28 d结束处死日止;免疫组及非免疫组大鼠每天腹腔注射等量0.9%氯化钠溶液.对各组大鼠进行神经功能缺损评分、病理学及免疫组织化学检查.结果 α-LA干预组的EAE发病率为5/11,显著低于免疫组的9/11(P<0.01).α-LA干预组大鼠免疫后第14天及第16～28天的神经功能缺损评分显著低于免疫组(P值均<0.05).α-LA干预组大鼠脑组织切片脱髓鞘病灶数为(3.85±1.21)个,脊髓组织切片病灶数为(4.26±2.65)个,均显著少于免疫组的(9.09±5.61)和(14.45±5.10)个(P值均<0.05).免疫组织化学髓鞘碱性蛋白(MBP)染色也显示,α-LA干预组病理切片的髓鞘松散、脱失明显轻于免疫组.结论 α-LA能显著改善EAE大鼠的神经功能,干预EAE的发病.
目的 研究α-硫辛痠(α-LA)對實驗性自身免疫性腦脊髓炎(EAE)大鼠模型榦預的有效性,探討α-LA臨床治療多髮性硬化的可能性.方法 Wistar大鼠30隻,其中22隻製作EAE模型,分為α-LA榦預組(11隻)及免疫組(11隻),另8隻為非免疫組.α-LA榦預組大鼠于免疫噹天開始每天1次腹腔註射α-LA(100 mg/kg),至實驗28 d結束處死日止;免疫組及非免疫組大鼠每天腹腔註射等量0.9%氯化鈉溶液.對各組大鼠進行神經功能缺損評分、病理學及免疫組織化學檢查.結果 α-LA榦預組的EAE髮病率為5/11,顯著低于免疫組的9/11(P<0.01).α-LA榦預組大鼠免疫後第14天及第16～28天的神經功能缺損評分顯著低于免疫組(P值均<0.05).α-LA榦預組大鼠腦組織切片脫髓鞘病竈數為(3.85±1.21)箇,脊髓組織切片病竈數為(4.26±2.65)箇,均顯著少于免疫組的(9.09±5.61)和(14.45±5.10)箇(P值均<0.05).免疫組織化學髓鞘堿性蛋白(MBP)染色也顯示,α-LA榦預組病理切片的髓鞘鬆散、脫失明顯輕于免疫組.結論 α-LA能顯著改善EAE大鼠的神經功能,榦預EAE的髮病.
목적 연구α-류신산(α-LA)대실험성자신면역성뇌척수염(EAE)대서모형간예적유효성,탐토α-LA림상치료다발성경화적가능성.방법 Wistar대서30지,기중22지제작EAE모형,분위α-LA간예조(11지)급면역조(11지),령8지위비면역조.α-LA간예조대서우면역당천개시매천1차복강주사α-LA(100 mg/kg),지실험28 d결속처사일지;면역조급비면역조대서매천복강주사등량0.9%록화납용액.대각조대서진행신경공능결손평분、병이학급면역조직화학검사.결과 α-LA간예조적EAE발병솔위5/11,현저저우면역조적9/11(P<0.01).α-LA간예조대서면역후제14천급제16～28천적신경공능결손평분현저저우면역조(P치균<0.05).α-LA간예조대서뇌조직절편탈수초병조수위(3.85±1.21)개,척수조직절편병조수위(4.26±2.65)개,균현저소우면역조적(9.09±5.61)화(14.45±5.10)개(P치균<0.05).면역조직화학수초감성단백(MBP)염색야현시,α-LA간예조병리절편적수초송산、탈실명현경우면역조.결론 α-LA능현저개선EAE대서적신경공능,간예EAE적발병.
Objective To explore the efficacy of α-lipoic acid (α-LA) in treating rat with experimental autoimmune encephalomyelitis (EAE), and to discuss the feasibility of using α-LA for treatment of multiple sclerosis (MS). Methods Twenty-two rats with EAE were randomly divided into the treatment group (n = 11) and immunization group (n = 11); another 8 rats served as non-immunization controls (n = 8). The treatment group was given daily intraperitoneal α-LA (100 mg/kg) from the 1~(st) day of research till the 28~(th) day when the animals were sacrificed; the immunization group and non-immunization group received equal volume of normal saline. Meanwhile, we also observed the clinical neurological scores and the pathology, immunohistochemistry outcomes of all rats. Results The treatment group had a EAE incidence of 5(5/11), which was significantly lower than that in the immunization group (9[9/11], P<0. 01). The clinical neurological score of the treatment group was significantly lower than that of the immunization group on the 14~(th),16~(th)-28~(th) day (P<0.05). The demyelinating lesions were 3.85±1.21 in the brain and 4.26 ± 2.65 in the spinal cord of the treatment group, which were significantly lower than those of the immunization group (9.09±5.61 in brain and 14.45±5.10 in the spinal cord, P<0. 05). Immunohistochemistry examination showed that demyelinating lesions of the treatment group were obviously slighter than those of the immunization group. Conclusion α-LA can greatly improve the clinical neurological functions of rat EAE model, preventing the progression of EAE.
