苦参素对实验性自身免疫脑脊髓炎大鼠的干预效果及其机制

摘要

目的 探讨苦参素对实验性自身免疫脑脊髓炎(EAE)大鼠的干预效果及其可能机制.方法 将30只雌性大鼠随机分为对照组、EAE组及苦参素组,每组10只.以豚鼠脊髓匀浆和完全福氏佐剂制备免疫抗原.给予EAE组及苦参素组大鼠注射免疫抗原以建立EAE大鼠模型,而对照组注射等量生理盐水.苦参素组给予苦参素胶囊灌胃,对照组及EAE组给予等量生理盐水灌胃.观察各组的发病情况,并于发病高峰期进行神经功能障碍评分,检测静脉血CD4 +、CD8 +的比例及CD4 +/CD8 +值.结果 EAE组及苦参素组大鼠均出现EAE症状,但苦参素组症状较EAE组轻;EAE组大鼠发病潜伏期短于苦参素组,进展期长于苦参素组,发病高峰期的神经功能障碍评分高于苦参素组(P＜0.05);对照组、苦参素治疗组、EAE组CD4 +、CD8 +淋巴细胞比例依次降低(P＜0.05),而CD4 +/CD8 +值依次升高(P＜0.05).结论 苦参素可能通过调节CD4 +、CD8 +淋巴细胞比例,以改善免疫功能,从而减轻EAE大鼠的症状.%Objective To explore the effect and its potential mechanism of oxymatrine on rats with experimental autoimmune encephalomyelitis (EAE). Methods Thirty female rats were randomly divided into normal control group,EAE control group and oxymatrine group,with 10 rats in each group.Rats in the EAE control group and oxymatrine group were injected with immunogen,produced by Guinea pig spinal cord homogenate and complete Freund′s adjuvant,to develop the rat model of EAE,while in the control group with an equivalent volume of normal saline.The oxymatrine group was given oxymatrine capsule by gavage,and the control group and EAE group were given an equivalent volume of normal saline by gavage.The incidence of the disease was observed in each group,the neurological dysfunction score was obtained at the peak of onset,and the proportions of venous blood CD4 +and CD8 +as well as the value of CD4 +to CD8 +was detected.Results Clinical symptoms of EAE were observed in the rats of the EAE group and oxymatrine group,milder in the oxymatrine group than those in the EAE group;the latency of disease onset was shorter,the disease progression was longer,and the neurological dysfunction score at the peak of onset was higher in the EAE group compared to those in the oxymatrine group(P＜0.05);the proportions of lymphocytes CD4 +and CD8 +decreased in turn while the value of CD4 +to CD8 +increased in turn in the control group,oxymatrine group and EAE group(P＜0.05).Conclusion Oxymatrine can improve the immune function by adjusting the proportions of lymphocytes CD4 +and CD8 +,thus alleviating the clinical symptoms of EAE rats.