氨基胍对白介素-1β损伤的离体大鼠胰岛细胞的保护作用  

The protective effects of aminoguanidine against interleukin-1β-induced destruction of isolated rat pancreatic islets of Langerhans

作　　者：陈宏[1] 蔡德鸿[1] 王梅[1] 刘宏[1] 叶仁青[1] 

机构地区：[1]第一军医大学附属珠江医院内分泌科

出　　处：《中国病理生理杂志》1999年第7期628-630,共3页Chinese Journal of Pathophysiology

摘　　要：目的：观察氨基胍（ＡＧ）对白细胞介素－１β（ＩＬ－１β）诱导的胰岛细胞损害的作用。方法：应用体外单层培养的大鼠胰岛细胞，分别检测ＩＬ－１β、ＡＧ及其联合对胰岛细胞亚硝酸盐生成、胰岛素分泌以及胞内ＤＮＡ、胰岛素含量和细胞活性的影响。结果：以ＩＬ－１β诱导，胰岛细胞亚硝酸盐生成量显著增加；同时胰岛素基础分泌以及葡萄糖刺激的胰岛素释放均明显减少；胰岛细胞内ＤＮＡ、胰岛素含量及细胞活性（ＭＴＴ值）均显著下降（均Ｐ＜００１）；ＡＧ能阻断这些抑制效应（均Ｐ＜０．０１）。结论：ＩＬ－１β通过一氧化氮（ＮＯ）介导对胰岛细胞有细胞活性抑制和毒性效应。ＡＧ可能是一种有效的ｉＮＯＳ抑制剂，通过阻断ＮＯ生成起到细胞保护作用。AIM:The effects of aminoguanidine (AG) on interleukin-1β-induced destruction of isolated rat pancreatic islets of Langerhans were obseved. METHODS:Isolated pancreatic islet cells from SD rat were cultured in monolayer in vitro. Nitrite production, insulin release, islet cell DNA and insulin content, and cell activity (MTT assay) in rat pancreatic islet cells incubated with IL-1β, AG, singly and in combination, were measured. RESULTS:IL-1β induced a significant increase in nitrite prodution, inhibited the medium insulin accumulation and the glucose-stimulated insulin release, and decreased islet cell DNA and insulin content and MTT reduction ( P <0.01), which were blocked by AG( P <0.01). CONCLUSION: The cytotoxicity of IL-1β on pancreatic islets might be mediated by nitric oxide (NO), and that AG prevented IL-1β-induced destruction of pancreatic islets as a inhibitor of NO formation.

关 键 词：一氧化氮 糖尿病 IL-1β 糖尿病 IDDM 氨基胍 

分 类 号：R587.102[医药卫生—内分泌]