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首页> 外文期刊>The Journal of Nutritional Biochemistry >Effects of physiological quercetin metabolites on interleukin-1 beta-induced inducible NOS expression
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Effects of physiological quercetin metabolites on interleukin-1 beta-induced inducible NOS expression

机译：槲皮素生理代谢产物对白介素1β诱导型NOS表达的影响

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摘要

Cytokines released by inflammatory cells around the pancreatic islets are implicated in the pathogenesis of diabetes mellitus. Specifically, interleukin-1 beta (IL-1 beta ) is known to be involved in islet beta -cell damage by activation of nuclear factor- kappa B (NF- kappa B)-mediated inducible nitric oxide synthase (iNOS) gene expression. Though most flavonoids are shown to have various beneficial effects, little is known about the anti-inflammatory effects of their metabolites. Therefore, we investigated the effects of quercetin and its metabolites quercetin 3'-sulfate, quercetin 3-glucuronide and isorhamnetin 3-glucuronide on IL-1 beta -stimulated iNOS gene expression in RINm5F beta -cells. The nitrite level, iNOS protein and its mRNA expression levels and iNOS promoter activity were measured. In addition, I kappa B alpha protein phosphorylation, nuclear translocation of nuclear factor- kappa B (NF- kappa B) and NF- kappa B DNA binding activity were determined. Adenosine 5'-triphosphate disodium salt-induced insulin release was also measured. Quercetin significantly reduced IL-1 beta -induced nitrite production, iNOS protein and its mRNA expression levels, and it also inhibited IL-1 beta -induced I kappa B alpha phosphorylation, NF- kappa B activation and iNOS promoter activity. Additionally, quercetin significantly restored the inhibition of insulin secretion by IL-1 beta . Meanwhile, quercetin metabolites did not show any effect on IL-1 beta -induced iNOS gene expression and also on insulin secretion. Therefore, in terms of iNOS expression mechanism, dietary ingestion of quercetin is unlikely to show anti-inflammatory effects in rat islet beta -cells exposed to IL-1 beta .
机译：胰岛周围的炎性细胞释放的细胞因子与糖尿病的发病有关。具体地，已知白介素-1β（IL-1β）通过激活核因子-κB（NF-κB）介导的诱导型一氧化氮合酶（iNOS）基因表达而参与胰岛β-细胞损伤。尽管大多数类黄酮显示出各种有益作用，但对其代谢产物的抗炎作用知之甚少。因此，我们研究了槲皮素及其代谢产物槲皮素3'-硫酸盐，槲皮素3-葡萄糖醛酸苷和异鼠李素3-葡萄糖醛酸苷对RINm5Fβ细胞中IL-1β刺激的iNOS基因表达的影响。测量亚硝酸盐水平，iNOS蛋白及其mRNA表达水平和iNOS启动子活性。另外，测定了IκBα蛋白的磷酸化，核因子κB（NF-κB）的核易位和NF-κBDNA结合活性。还测量了腺苷5'-三磷酸二钠盐诱导的胰岛素释放。槲皮素显着降低了IL-1β诱导的亚硝酸盐生成，iNOS蛋白及其mRNA表达水平，并且还抑制了IL-1β诱导的IκBα磷酸化，NFκB活化和iNOS启动子活性。此外，槲皮素可显着恢复IL-1β对胰岛素分泌的抑制作用。同时，槲皮素代谢物对IL-1β诱导的iNOS基因表达以及胰岛素分泌均无影响。因此，就iNOS表达机制而言，槲皮素的饮食摄入不太可能在暴露于IL-1β的大鼠胰岛β细胞中显示出抗炎作用。

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