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目的 观察一氧化氮（ＮＯ）在白介素－１β（ＩＬ－１β）诱导的胰岛细胞损伤机制中的作用。方法 应用体外单层培养的大鼠胰岛细胞，分别检测ＩＬ－１β、一氧化氮合酶抑制剂ＮＧ－单甲基－Ｌ－精氨酸（Ｌ－ＮＭＭＡ）（１ｍ ｍ ｏｌ／Ｌ）、胰岛细胞保护剂尼克酰胺（ＮＡ）（１０，２０ｍ ｍ ｏｌ／Ｌ）及ＩＬ－１β分别与Ｌ－ＮＭＭＡ、ＮＡ联合对胰岛细胞亚硝酸盐生成、胰岛素分泌以及胰岛细胞内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（Ｐ均＜ ０．００１）；Ｌ－ＮＭＭＡ、较高浓度的ＮＡ（２０ｍ ｍ ｏｌ／Ｌ）能阻断这些抑制作用（Ｐ均＜ ０．００１）。而较低浓度的ＮＡ（１０ｍ ｍ ｏｌ／Ｌ）虽不能阻断ＩＬ－１β诱导的ＮＯ生成和对葡萄糖刺激的胰岛素释放的抑制作用，仍呈现对ＩＬ－１β其它抑制作用的保护性效应（Ｐ均＜ ０．００１）。结论 ＮＯ虽然参与ＩＬ－１β诱导的对胰岛细胞的损害过程，但可能并不是唯一的效应分子
Objective To investigate the role of nitric oxide (NO) in the mechanism of interleukin-1β (IL-1β) -induced islet cell injury. Methods The rat islet cells cultured in vitro were cultured and the expressions of IL-1β, N-monomethyl-L-arginine (L-NMMA) (1 m mol / L) Nitric oxide (NOS) (10,20 m mol / L) and IL-1β were respectively combined with L-NMMA and NA to produce nitrite, insulin secretion, DNA content, insulin content and cell viability in islet cells Impact. Results IL-1βinduced significantly increased nitrite production in pancreatic islet cells. Both basal insulin secretion and glucose-stimulated insulin release decreased significantly. The contents of DNA, insulin and MTT in pancreatic islets decreased significantly (P All <0.001). L-NMMA and higher concentration of NA (20 m mol / L) blocked these inhibitory effects (all P <0.001). However, low concentrations of NA (10 m mol / L) did not block the IL-1β-induced NO production and glucose-stimulated insulin release, but still showed protective effects on other inhibitory effects of IL-1β (P All <0.001). Conclusion Although NO is involved in the process of islet cell damage induced by IL-1β, it may not be the only effector molecule