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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >EVIDENCE OF AUTOCRINE MODULATION OF MACROPHAGE NITRIC OXIDE SYNTHASE BY ALPHA-MELANOCYTE-STIMULATING HORMONE
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EVIDENCE OF AUTOCRINE MODULATION OF MACROPHAGE NITRIC OXIDE SYNTHASE BY ALPHA-MELANOCYTE-STIMULATING HORMONE

机译：α-黑素细胞刺激激素自噬调节巨噬细胞一氧化氮合酶的证据

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摘要

alpha-Melanocyte-stimulating hormone (alpha-MSH) is a potent inhibitory agent in all major forms of inflammation. To identify a potential mechanism of antiinflammatory action of alpha-MSH, we tested its effects on production of nitric oxide (NO), believed to be a mediator common to all forms of inflammation. We measured NO and alpha-MSH production in RAW 264.7 cultured murine macrophages stimulated with bacterial lipopolysaccharide and interferon gamma. alpha-MSH inhibited production of NO, as estimated from nitrite production and nitration of endogenous macrophage proteins. This occurred through inhibition of production of NO synthase II protein; steady-state NO synthase II mRNA abundance was also reduced. alpha-MSH increased cAMP accumulation in RAW cells, characteristic of alpha-MSH receptors in other cell types. RAW cells also expressed mRNA for the primary alpha-MSH receptor (melanocortin 1). mRNA for proopiomelanocortin, the precursor molecule of alpha-MSH, was expressed in RAW cells, and tumor necrosis factor ar increased production and release of alpha-MSH. These results suggest that the proinflammatory cytokine tumor necrosis factor alpha can induce macrophages to increase production of alpha-MSH, which then becomes available to act upon melanocortin receptors on the same cells. Such stimulation of melanocortin receptors could modulate inflammation by inhibiting the production of NO. The results suggest that alpha-MSH is an autocrine factor in macrophages which modulates inflammation by counteracting the effects of proinflammatory cytokines. [References: 47]
机译：α-黑素细胞刺激激素（α-MSH）是所有主要炎症形式的有效抑制剂。为了确定α-MSH抗炎作用的潜在机制，我们测试了其对一氧化氮（NO）产生的影响，据信一氧化氮是所有形式的炎症常见的介质。我们测量了用细菌脂多糖和干扰素γ刺激的RAW 264.7培养的鼠巨噬细胞中NO和α-MSH的产生。从亚硝酸盐的产生和内源性巨噬细胞蛋白的硝化作用估计，α-MSH抑制NO的产生。这是通过抑制NO合酶II蛋白质的产生而发生的。稳态NO合酶II mRNA的丰度也降低了。 alpha-MSH增加了RAW细胞中cAMP的积累，这是其他细胞类型中alpha-MSH受体的特征。 RAW细胞还表达了主要的α-MSH受体（黑皮质素1）的mRNA。 α-MSH的前体分子proopiomelanocortin的mRNA在RAW细胞中表达，肿瘤坏死因子增加了α-MSH的产生和释放。这些结果表明促炎性细胞因子肿瘤坏死因子α可以诱导巨噬细胞增加α-MSH的产生，然后可用于对相同细胞上的黑皮质素受体起作用。黑色素皮质激素受体的这种刺激可以通过抑制NO的产生来调节炎症。结果表明，α-MSH是巨噬细胞中的自分泌因子，可通过抵消促炎细胞因子的作用来调节炎症。 [参考：47]

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