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首页> 外文期刊>American Journal of Physiology >PPARgamma is not required for the inhibitory actions of PGJ_2 on cytokine signaling in pancreatic beta-cells
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PPARgamma is not required for the inhibitory actions of PGJ_2 on cytokine signaling in pancreatic beta-cells

机译:PGJ_2对胰腺β细胞中细胞因子信号传导的抑制作用不需要PPARgamma

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摘要

Peroxisome proliferator-activated receptor (PPAR)7 agonists, such as 15-deoxy-DELTA~(12,14)-prostaglandin J_2 (PGJ_2) and troglitazone, have been shown to elicit anti-inflammatory effects in pancreatic beta-cells that include inhibition of cytokine-stimulated inducible nitric oxide synthase (iNOS) gene expression and production of nitric oxide. In addition, these ligands impair IL-1-induced NF-KB and MAPK as well as IFN-7-stimulated signal transducer and activator of transcription (STAT)l activation in beta-cells. The purpose of this study was to determine if PPAR7 activation participates in the anti-inflammatory actions of PGJ_2 in beta-cells.
机译:过氧化物酶体增殖物激活受体(PPAR)7激动剂,例如15-脱氧-DELTA〜(12,14)-前列腺素J_2(PGJ_2)和曲格列酮,已显示在胰腺β细胞中引起抗炎作用,包括抑制作用细胞因子刺激的诱导型一氧化氮合酶(iNOS)基因表达与一氧化氮产生的关系。此外,这些配体还损害了IL-1诱导的NF-KB和MAPK以及IFN-7刺激的β细胞中信号转导和转录激活剂(STAT)1的激活。这项研究的目的是确定PPAR7激活是否参与β细胞中PGJ_2的抗炎作用。

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