Southern C, Schulster D, Green I C
Department of Biochemistry, University of Sussex, Brighton, UK.
FEBS Lett. 1990 Dec 10;276(1-2):42-4. doi: 10.1016/0014-5793(90)80502-a.
Inhibition of glucose-induced insulin secretion by interleukin-1 beta (IL-1 beta), or IL-1 beta plus tumour necrosis factor-alpha (TNF-alpha), was less marked when rat islets of Langerhans were cultured for 12 h with these cytokines in L-arginine-free medium as opposed to medium containing L-arginine (1 mM). Inhibition of secretion by IL-1 beta was further alleviated when islets were maintained in L-arginine-free medium supplemented with N-omega-nitro-L-arginine methyl ester (NAME), while synergism between IL-1 beta plus TNF-alpha was completely abolished. Tissue culture medium nitrite levels were raised in islets treated with IL-1 beta or TNF-alpha (48 h). Cytokine-stimulated nitrite production was not observed in islets cultured with NAME (1 mM). In conclusion, an L-arginine-dependent nitric oxide generating mechanism is involved in the inhibition of insulin secretion by IL-1 beta, and accounts for the phenomenon of synergism between IL-1 beta and TNF-alpha.
与含有L-精氨酸（1 mM）的培养基相比，当大鼠胰岛在无L-精氨酸的培养基中与白细胞介素-1β（IL-1β）或IL-1β加肿瘤坏死因子-α（TNF-α）一起培养12小时时，葡萄糖诱导的胰岛素分泌受到的抑制作用不那么明显。当胰岛在补充有N-ω-硝基-L-精氨酸甲酯（NAME）的无L-精氨酸培养基中培养时，IL-1β对分泌的抑制作用进一步减轻，而IL-1β加TNF-α之间的协同作用则完全消失。用IL-1β或TNF-α处理的胰岛（48小时）中，组织培养基亚硝酸盐水平升高。在用NAME（1 mM）培养的胰岛中未观察到细胞因子刺激的亚硝酸盐产生。总之，一种依赖L-精氨酸的一氧化氮生成机制参与了IL-1β对胰岛素分泌的抑制作用，并解释了IL-1β与TNF-α之间的协同作用现象。
