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黑米提取物通过下调NF-κB和AP-1信号通路抑制RAW 264.7巨噬细胞中的炎症反应。

Suppression of Inflammatory Responses by Black Rice Extract in RAW 264.7 Macrophage Cells via Downregulation of NF-kB and AP-1 Signaling Pathways.

作者信息

Limtrakul Pornngarm, Yodkeeree Supachai, Pitchakarn Pornsiri, Punfa Wanisa

机构信息

Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand E-mail :

出版信息

Asian Pac J Cancer Prev. 2015;16(10):4277-83. doi: 10.7314/apjcp.2015.16.10.4277.

Abstract

Anthocyanin, a phenolic compound, has been reported to have an anti-inflammatory effect against lipopolysaccharide (LPS) induced changes in immune cells. However, little is known about the molecular mechanisms underlying its anti-inflammatory effects. Few research studies have concerned the anti-inflammation properties of colored rice extract as a functional material. Therefore, the purpose of this study was to examine anti-inflammatory effects of the polar fraction of black rice whole grain extracts (BR-WG-P) that features a high anthocyanin content. Our results showed that BR-WG-P significantly inhibited LPS-induced pro- inflammatory mediators, including production of NO and expression of iNOS and COX-2. In addition, secretion of pro-inflammatory cytokines including TNF-α and IL-6 was also significantly inhibited. Moreover, BR-WG-P and anthocyanin inhibited NF-kB and AP-1 translocation into the nucleus. BR-WG-P also decreased the phosphorylation of ERK, p38 and JNK in a dose dependent manner. These results suggested that BR-WG-P might suppress LPS-induced inflammation via the inhibition of the MAPK signaling pathway leading to decrease of NF-kB and AP-1 translocation. All of these results indicate that BR-WG-P exhibits therapeutic potential associated with the anthocyanin content in the extract for treating inflammatory diseases associated with cancer.

摘要

花青素是一种酚类化合物,据报道其对脂多糖(LPS)诱导的免疫细胞变化具有抗炎作用。然而,其抗炎作用的分子机制尚不清楚。很少有研究关注有色米提取物作为功能材料的抗炎特性。因此,本研究的目的是检测富含花青素的黑米全谷物提取物的极性部分(BR-WG-P)的抗炎作用。我们的结果表明,BR-WG-P显著抑制LPS诱导的促炎介质,包括NO的产生以及iNOS和COX-2的表达。此外,包括TNF-α和IL-6在内的促炎细胞因子的分泌也受到显著抑制。此外,BR-WG-P和花青素抑制NF-κB和AP-1向细胞核的转位。BR-WG-P还以剂量依赖性方式降低ERK、p38和JNK的磷酸化。这些结果表明,BR-WG-P可能通过抑制MAPK信号通路来抑制LPS诱导的炎症,从而导致NF-κB和AP-1转位减少。所有这些结果表明,BR-WG-P在治疗与癌症相关的炎症性疾病方面具有与提取物中花青素含量相关的治疗潜力。

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