重组人IL-6对NOD小鼠IDDM发病的影响及机制研究

被引：1

作者：

向明Ferdinando icoletti ^{[1
]}

机构：

[1] 华中科技大学同济药学院药理学教研室

[2] Dept of Microbiology

[3] University of Milan

来源：

中国药理学通报 | 2003年 / 08期

关键词：

Ⅰ型糖尿病; 白细胞介素6; NOD小鼠; 环磷酰胺;

D O I：

暂无

中图分类号：

R587.1 [糖尿病];

学科分类号：

摘要：

目的　探讨重组人白细胞介素 6(rhIL 6)对NOD小鼠自发性和环磷酰胺 (CY)诱发性Ⅰ型糖尿病 (IDDM)的影响及相关机制。方法　通过观察NOD小鼠用药后血糖和尿糖水平、胰腺组织病理学特征 ,及血清抗CD3抗体、LPS诱导的炎症因子IFN γ、TNF α水平的变化 ,以及CY诱导ID DM发生率 ,确定rhIL 6的抗IDDM作用。结果　 4wk龄♀NOD小鼠连续注射rhIL 6 1 6wk后 ,胰岛炎即胰腺淋巴细胞、单核细胞浸润明显减少 ,糖尿病的发病率明显降低(33 % )。与空白对照组相比 ,血清中炎症因子IFN γ、TNF α水平也呈显著的下降趋势。 1 2wk龄NOD小鼠连续 8wk应用rhIL 6 ,糖尿病发生率则无明显变化 ,且实验中未观察到rhIL 6对CY诱发IDDM的保护作用。结论　rhIL 6早期预防用药可降低NOD小鼠自发性IDDM的发生 ,该保护作用可能与其降低炎症因子TNF α、IFN γ分泌有关

引用

页码：917 / 919

页数：3

共 10 条

[1]

An update on cytokines in the pathogenesis of IDDM. Rabinovitch A. Diabetes Metabolism Reviews . 1998

[2]

Immunolatory and cytokine imbalances in the pathogenesis of IDDM. Rabinovitch A. Therapeutic intervention by immunostimulation? Diabetes . 1994

[3]

Insulin-dependent diabetes mellitus as an autoimmune disease. Bach JF. Endocrine Research . 1994

[4]

Th1 to Th2 cytokine shifts in NOD mice: Sometimes an outcome, rather than the cause of diabetes resistance elicited by immunostimulation. Serreze DV,Harold D,Cristina MP et al. J Immunology .

[5]

T cell activation-associated hepatic injury: Mediation by TNF and protection by IL-6. Mizuhara H,O’Neill E,Seki N et al. The Journal of Experimental Medicine . 1994

[6]

Correlations and Interactions in the production of IL-6, IL-1 and TNF in human blood mononuclear cells: IL-6 suppresses IL-1 and TNF. Schindler R,Mancilla J,Endres S et al. Blood . 1990

[7]

IL-6 as an anti-inflammatory cytokine: Induction of circulating IL-1 receptor antagonist and sTNF receptor p55. Tilg H,Trehu E,Michael B et al. Blood . 1994

[8]

Genetic protection from the inflammatory disease type 1 diabetes in humans and animal models. John AT,Linda SW. Immunity . 2001

[9]

Tolerogenic strategies to halt or prevent type 1 diabetes. Cook A,Jenny MP,Nicole MP. Nature Immunology . 2001

[10]

Type 1 diabetes-predisposing MHC alleles influence the selection of GAD65-specific T cells in a transgenic model. Abraham RS,Li W,Marietta E et al. J Immunology . 2001

← 1 →