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姜黄素可降低白塞病患者 M1 巨噬细胞中白细胞介素 1β 的表达及白细胞介素 6 和肿瘤坏死因子 α 的产生。

Curcumin reduces the expression of interleukin 1β and the production of interleukin 6 and tumor necrosis factor alpha by M1 macrophages from patients with Behcet's disease.

机构信息

a Rheumatology Research Center , Tehran University of Medical Sciences , Tehran , Iran.

b Department of Cell and Molecular Biology , University of Tehran , Tehran , Iran.

出版信息

Immunopharmacol Immunotoxicol. 2018 Aug;40(4):297-302. doi: 10.1080/08923973.2018.1474921. Epub 2018 May 28.

Abstract

OBJECTIVE

Behcet's disease (BD) is an auto-inflammatory disorder. Curcumin as a bio-active agent has anti-inflammatory properties. Effects of curcumin on the pathogenesis of BD are still not clear. In this study, we investigated the effect of curcumin on the inflammatory cytokines expression and production in M1 macrophages from BD patients compared with healthy controls.

METHODS

Monocytes were collected from 10 healthy controls and 20 active BD patients, differentiated to macrophages by macrophage-colony stimulating factor for 7 d. Macrophages were then treated with interferon gamma, lipopolysaccharide, and curcumin (10 or 30 µg/ml) for 24 h. Analysis of tumor necrosis factor-alpha (TNFα), interleukin 1β (IL-1β), and IL-6 mRNA expression and protein production was performed using SYBR Green qPCR and ELISA method.

RESULTS

Treatment with 30 µg/ml curcumin significantly down-regulated mRNA expression of IL-1β (p < .05) and protein production of IL-6 (p < .05) in M1 macrophages from BD patients but not in M1 macrophage from controls. Treatment with 30 µg/ml curcumin also significantly diminishes the protein production of TNFα in BD patients (p < .01) and healthy controls (p < .05) M1 macrophages.

CONCLUSIONS

We demonstrated that curcumin can inhibit the expression and production of inflammatory cytokines in M1 macrophages from BD patients. Our results suggest that curcumin can modulate inflammatory signaling more specifically in macrophages from BD patients than healthy macrophages.

摘要

目的

贝切特病(BD)是一种自身炎症性疾病。姜黄素作为一种生物活性物质具有抗炎特性。姜黄素对 BD 发病机制的影响尚不清楚。在这项研究中,我们研究了姜黄素对来自 BD 患者和健康对照的 M1 巨噬细胞中炎症细胞因子表达和产生的影响。

方法

从 10 名健康对照者和 20 名活动期 BD 患者中收集单核细胞,用巨噬细胞集落刺激因子分化为巨噬细胞 7 天。然后用干扰素 γ、脂多糖和姜黄素(10 或 30μg/ml)处理巨噬细胞 24 小时。采用 SYBR Green qPCR 和 ELISA 法分析肿瘤坏死因子-α(TNFα)、白细胞介素 1β(IL-1β)和 IL-6 mRNA 表达和蛋白产生。

结果

30μg/ml 姜黄素处理显著下调了 BD 患者 M1 巨噬细胞中 IL-1β 的 mRNA 表达(p<0.05)和 IL-6 的蛋白产生(p<0.05),但对对照者的 M1 巨噬细胞无影响。30μg/ml 姜黄素处理还显著降低了 BD 患者(p<0.01)和健康对照者(p<0.05)M1 巨噬细胞中 TNFα 的蛋白产生。

结论

我们证明了姜黄素可以抑制 BD 患者 M1 巨噬细胞中炎症细胞因子的表达和产生。我们的结果表明,姜黄素可以更特异性地调节 BD 患者巨噬细胞中的炎症信号,而不是健康巨噬细胞。

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