尼克酰胺对白介素-1β损伤的离体大鼠胰岛细胞的保护作用

摘要/Abstract

摘要： 目的观察尼克酰胺(NA)对白细胞介素-ip(IL-1(3)诱导的胰岛细胞损害的保护作用。方法应用体外单层培养的大鼠胰岛细胞,分别检测IL-1(3, NA(10, 20 mmol/L)及其联合对胰岛细胞亚硝醆盐生成,肤岛素分泌以及胞内DNA,胰岛素含量和细胞活性的影响。结果由IL-1β谓导的肤岛細胞亚硝醆盐生成量显著增加,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,狹岛素含量及细胞活性（MTT值）均显著下降（P均<0.001);较高浓度及其的NA(20 mmol/1,)能阻断这些抑制作用（P均<0.001);而较低浓度的NA（10 mmol/L)虽不能阻断IL-1β诱导的NO生成对葡萄糖刺激的肤岛素释放的抑制作用,但对IL-lβ介导的其它抑制作用仍呈现保护性故应（P均<0.01)。结论一氧化氮(NO)虽然参与IL-lβ诱导的胰岛细胞的损害过程,但可能不是唯一的故应分子。NA可能通过包括抑制NO生成等多方面机制,实现对IL-1β诱导的胰岛細胞损害的保护作用。

关键词: 尼克酰胺, 白细胞介素-1, 一氧化氮, 胰岛细胞

Abstract: Aim The effects of nicotinamide (NA) on interleukin-ip-induced destruction of isolated rat pancreatic islets of Langerhans were observed. Method 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 or/and NA (10,20 mmol/L),were measured. Results IL-lβinduced a significant increase in nitrite production, inhibited the medium insulin accumulation and the glucose-stimulated insulin, release, and decreased islet cell DNA insulin content and MTT(P<0.001).The inhibitory activities were blocked by NA in a higher dose (20 mmol/L) (P<0.001) while in a lover dose. NA (10 mmol/L) prevented the IL-lβ-induced cytotoxic effects without affecting nitrite production and the glucose-stimulated insulin release. Conclusion IL-lβ-induced nitric oxide (NO) production alone is insufficient to account for the IL-lβ-mediated islet p-cell destruction. Mechanisms of other action of the IL-1β may be involved. There may be a variety of mechanisms the protective effects of NA against cytotoxic action of IL-1β, including inhibition of NO Production, which may be related to exposure concentration of NA.

Key words: nicotinamide, interleukin-1, nitric oxide, islets of Langerhans

中图分类号:

R977.15

陈宏, 蔡德鸿, 王梅. 尼克酰胺对白介素-1β损伤的离体大鼠胰岛细胞的保护作用[J]. 中国临床药理学与治疗学, 1999, 4(1): 36-39.

CHEN Hong, CAI De-Hong, WANG Mei. Protective effects of nicotinamide against interleukin-1β-induced destruction of isolated rat pancreatic islets of Langerhans[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 1999, 4(1): 36-39.

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