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短期口服阿司匹林可增加全血培养物中白细胞介素-18诱导的γ干扰素生成。

A short course of oral aspirin increases IL-18-induced interferon-gamma production in whole blood cultures.

作者信息

Netea M G, Puren A J, Dinarello C A

机构信息

Division of Infectious Diseases, B168, University of Colorado Health Sciences Center, 4200 East Ninth Ave., Denver, CO 80262, USA.

出版信息

Eur Cytokine Netw. 2000 Sep;11(3):379-82.

PMID:11022121
Abstract

The effect of aspirin on whole blood cytokine production was studied in six healthy volunteers. Four days after cessation of a 3-day regimen of 650 mg of oral aspirin, there was a 70% increase in interferon-gamma (IFN-gamma) production, stimulated by a combination of interleukin-18 (IL-18) plus lipopolysaccharide (p < 0.05). At this time, there was a 4-fold increase in the production of tumor necrosis factor-alpha (TNF-alpha) compared to pre-aspirin levels (p < 0.03). TNF-alpha and IFN-gamma production returned to pre-aspirin levels one month after the discontinuation of aspirin. Short-term aspirin treatment induces a significant increase in the production of these cytokines, probably through inhibition of prostaglandins. These data suggest a novel pathway through which long aspirin use reduces the risk of colon cancer, and may explain the effects of aspirin in inflammatory bowel disease.

摘要

在六名健康志愿者中研究了阿司匹林对全血细胞因子产生的影响。在停止服用650毫克口服阿司匹林的3天疗程后四天,白细胞介素-18(IL-18)加脂多糖联合刺激下的干扰素-γ(IFN-γ)产生增加了70%(p<0.05)。此时,肿瘤坏死因子-α(TNF-α)的产生与服用阿司匹林前的水平相比增加了4倍(p<0.03)。停用阿司匹林一个月后,TNF-α和IFN-γ的产生恢复到服用阿司匹林前的水平。短期阿司匹林治疗可能通过抑制前列腺素诱导这些细胞因子产生显著增加。这些数据提示了长期服用阿司匹林降低结肠癌风险的一条新途径,并可能解释阿司匹林在炎症性肠病中的作用。

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