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姜黄素可减轻银屑病患者促炎细胞因子干扰素 γ 和白细胞介素 17 的反应,从而增强其作为膳食免疫抑制剂的作用。

Curcumin mediates attenuation of pro-inflammatory interferon γ and interleukin 17 cytokine responses in psoriatic disease, strengthening its role as a dietary immunosuppressant.

机构信息

Department of Rheumatology and Clinical Immunology, University of Thessaly, Larissa, Greece.

Department of Neurology, Faculty of Medicine, School of Health Sciences, University of Thessaly, Larissa, Greece.

出版信息

Nutr Res. 2020 Mar;75:95-108. doi: 10.1016/j.nutres.2020.01.005. Epub 2020 Feb 27.

Abstract

Curcumin exhibits anti-inflammatory properties and has been used for centuries in traditional medicine and as dietary supplement. Data from clinical trials has strengthened the notion that curcumin may exert an anti-inflammatory and immunosuppressive role in patients with psoriatic disease, but its mode of action has remained elusive. We hypothesized that curcumin could inhibit interferon (IFN)-γ and interleukin (IL)-17 production in peripheral blood mononuclear cells from patients with psoriasis and psoriatic arthritis (PsA). To this end, we assessed the in vitro effect of curcumin on IFN-γ production by cluster differentiation (CD)4(+), CD8(+) T cells, natural killer (NK) and NKT cells and on IL-17 production by CD4(+) T cells from 34 patients with psoriatic disease (22 with psoriasis and 12 with PsA); 15 normal subjects were included as healthy controls. We also assessed the effect of curcumin on signal transducer and activator of transcription (STAT)3 activation. Curcumin significantly decreased, in a dose dependent manner, IFNγ-production by CD4(+) and CD8(+) T cells, and NK and NKT cells in patients with psoriatic disease and healthy controls. It also decreased IL-17 production by CD4(+) T cells (Th17). At the molecular level, curcumin increased STAT3 serine 727 phosphorylation intensity and p-STAT3(+) CD4(+) T cells in patients with PsA and psoriasis. In conclusion, curcumin in vitro inhibits pro-inflammatory IFN-γ and IL-17 production in psoriatic disease, and this may strengthen its role as a dietary immunosuppressant in patients with this disease.

摘要

姜黄素具有抗炎特性,在传统医学和膳食补充剂中已使用了数个世纪。来自临床试验的数据加强了这样一种观念,即姜黄素可能在患有银屑病性疾病的患者中发挥抗炎和免疫抑制作用,但它的作用机制仍难以捉摸。我们假设姜黄素可以抑制银屑病和银屑病关节炎(PsA)患者外周血单个核细胞中干扰素(IFN)-γ和白细胞介素(IL)-17 的产生。为此,我们评估了姜黄素对 34 例银屑病患者(22 例银屑病和 12 例 PsA)外周血 CD4+、CD8+T 细胞、自然杀伤(NK)和 NKT 细胞 IFN-γ产生以及 CD4+T 细胞 IL-17 产生的体外作用;15 名正常受试者作为健康对照。我们还评估了姜黄素对信号转导和转录激活因子(STAT)3 激活的影响。姜黄素以剂量依赖的方式显著降低了银屑病患者和健康对照者 CD4+和 CD8+T 细胞以及 NK 和 NKT 细胞的 IFN-γ产生。它还降低了 CD4+T 细胞(Th17)的 IL-17 产生。在分子水平上,姜黄素增加了 PsA 和银屑病患者中 STAT3 丝氨酸 727 磷酸化强度和 p-STAT3+CD4+T 细胞。总之,姜黄素在体外抑制了银屑病疾病中的促炎 IFN-γ和 IL-17 产生,这可能增强了它作为这种疾病患者膳食免疫抑制剂的作用。

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