摘要
ＮＯＤ鼠是人类胰岛素依赖型糖尿病的动物模型，其发病与自身免疫有关。环磷酰胺（ＣＰ）可以加速这一过程，使ＮＯＤ鼠糖尿病的发病率提高或提前。一些研究表明：ＮＯＤ鼠的淋巴细胞在淋巴细胞混合反应中（ＭＬＲ），在有或无刺激物的存在下，白细胞介素２（ＩＬ－２）的产量均明显低于正常鼠的淋巴细胞。该实验对注射了一次大剂量的ＣＰ（３００ｍｇ／ｋｇ体重）后的ＮＯＤ鼠试用了ＩＬ－２治疗。结果显示：对于年幼的ＮＯＤ鼠ＩＬ－２治疗１４无可以明显减轻注射ＣＰ后的胰岛破坏加速。病理检查显示三组胰岛炎严重程度积分分别为２９；８１；８８。ＩＬ－２处理组明显低于ＣｏｎＡ处理组与对照组。这个研究还显示，对于１２周龄的ＮＯＤ鼠，经１４天的ＩＬ－２治疗，可以完全预防ＣＰ诱导的糖尿病的发生。糖尿病发病率在ＩＬ－２组为０／１２；对照组为７／１２。但对已发病的ＮＯＤ鼠自发性糖尿病ＩＬ－２不能使其缓解。
Nonobese diabetic (NOD)mouse is a model of human insulin-dependent diabetes
mellitus(IDDM). Pan-creatic cell destruction in NOD mouse is mediated by autoimmune process
which can be accelerated by cyclophos-phamide (CP ).Many studies have showed that the
production of interleukin-2(IL-2) in mixed lymphocyte reaction(MLR ),with or without promotion,in
NOD mice is lower than that in normal controls. Six NOD mice,8-week-old,which were injected
with CP(300mg/kg one dose)were treated with IL- 2(36Ou/mouse/day for 14 days )and
werecompared with con A treatrnent (5ug/mouse/day for 14 days )and vehicle treatment. The
severity of insulitis inIL-2, CON A and Vehicle group was 31, 81 and 88 respectively (P<0.01).
Twelve NOD mice,12-week-old,treatedwith IL-2and compared with vehicle treatment to
investigate effect of IL-2on incidence of diabetes after CP.Theresults showed that 14
days'treatment with IL-2could completely prevent diabetes in NOD mice after CP. The dia-betes
incidence in IL-2group was0/12 and that in Vehicle group was 7/12(p<0.05).
出处
《中华微生物学和免疫学杂志》
CAS
CSCD
北大核心
1994年第3期168-172,共5页
Chinese Journal of Microbiology and Immunology
关键词
白细胞介素2
NOD
糖尿病
NOD
mouse
Insulin-dependent diabetes mellitus
Interleukin-2
Cyclophosphamide
