Nicolson A G, Haites N E, McKay N G, Wilson H M, MacLeod A M, Benjamin N
Department of Medicine and Therapeutics, University of Aberdeen Medical School, Foresterhill, Scotland.
Biochem Biophys Res Commun. 1993 Jun 30;193(3):1269-74. doi: 10.1006/bbrc.1993.1762.
Synthesis of nitric oxide (NO) has been implicated in the development of glomerulonephritis in animal models of the disease. Rat mesangial cells can be stimulated to express an inducible form of NO synthase (NOS) in vitro. Little is known however, about the pathway of induction in human mesangial cells. Here, we report that human mesangial cells require multiple cytokines, unlike rat mesangial cells which require only single stimulants, to produce NO. Our experiments suggest that both interleukin-1 beta (IL-1 beta) and interferon gamma (IFN-gamma) must be present together to elicit a response whilst tumour necrosis factor alpha (TNF-alpha) augments this. The production of nitrite, a stable end product of NO metabolism, was inhibited by NG-monomethyl-L-arginine (L-NMMA), L-nitro-arginine-methyl-ester (L-NAME), cycloheximide and the glucocorticoid dexamethasone.
一氧化氮（NO）的合成与该疾病动物模型中肾小球肾炎的发展有关。大鼠系膜细胞在体外可被刺激表达诱导型一氧化氮合酶（NOS）。然而，关于人系膜细胞中诱导途径的了解却很少。在此，我们报告，与人系膜细胞不同，大鼠系膜细胞仅需单一刺激物，而人系膜细胞需要多种细胞因子来产生NO。我们的实验表明，白细胞介素-1β（IL-1β）和干扰素γ（IFN-γ）必须同时存在才能引发反应，而肿瘤坏死因子α（TNF-α）可增强这种反应。NO代谢的稳定终产物亚硝酸盐的产生受到NG-单甲基-L-精氨酸（L-NMMA）、L-硝基精氨酸甲酯（L-NAME）、环己酰亚胺和糖皮质激素地塞米松的抑制。
