Background Inflammation is central to the pathogenesis of many diseases. Supplementation with selenium and coenzyme Q10 has been shown to reduce cardiovascular mortality, and increase cardiac function in elderly persons with a low intake of selenium. There are indications that one of the mechanisms of this positive effect is a decrease in inflammation. Methods Osteopontin, osteoprotegerin, sTNF receptor 1, sTNF receptor 2 and the tumor necrosis factor-like weak inducer of apoptosis called TWEAK, were determined in plasma after 6 months and 42 months in 219 community-living elderly persons, of whom 119 received supplements of selenium (200 μg/day) and coenzyme Q10 (200 mg/day), and 101 received a placebo. Repeated measures of variance were used to evaluate the levels, and the results were validated through ANCOVA analyses with adjustments for important covariates. Results Significantly lower concentrations of four of the five biomarkers for inflammation were observed as a result of the intervention with the supplements. Only TWEAK did not show significant differences. Conclusion In this sub-analysis of the intervention with selenium and coenzyme Q10 or placebo in an elderly community-living population, biomarkers for inflammation were evaluated. A significantly lower concentration in four of the five biomarkers tested could be demonstrated as a result of the supplementation, indicating a robust effect on the inflammatory system. The decrease in inflammation could be one of the mechanisms behind the positive clinical results on reduced cardiovascular morbidity and mortality reported earlier as a result of the intervention. The study is small and should be regarded as hypothesis-generating, but nonetheless adds important data about mechanisms presently known to increase the risk of clinical effects such as reduced cardiovascular mortality, increased cardiac function and better health-related quality of life scoring, as previously demonstrated in the active treatment group . Trial registration The intervention study was registered at Clinicaltrials.gov, and has the identifier NCT01443780 and registered on 09/30/2011.

中文翻译：

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通过干预硒和辅酶 Q10 降低炎症生物标志物浓度：骨桥蛋白、骨保护素、TNFr1、TNFr2 和 TWEAK 的亚分析。

背景炎症是许多疾病发病机制的核心。补充硒和辅酶 Q10 已被证明可降低硒摄入量低的老年人的心血管死亡率，并增加心脏功能。有迹象表明，这种积极作用的机制之一是炎症减少。方法 对 219 名社区老年人在 6 个月和 42 个月后血浆中的骨桥蛋白、骨保护素、sTNF 受体 1、sTNF 受体 2 和肿瘤坏死因子样弱凋亡诱导剂 TWEAK 进行测定，其中 119 人补充了硒（200 微克/天）和辅酶 Q10（200 毫克/天），101 人接受了安慰剂。重复测量方差用于评估水平，并通过 ANCOVA 分析验证了结果，并对重要协变量进行了调整。结果由于使用补充剂的干预，观察到五种炎症生物标志物中四种的浓度显着降低。只有 TWEAK 没有显示出显着差异。结论 在这项对老年人社区生活人群中硒和辅酶 Q10 或安慰剂干预的子分析中，评估了炎症的生物标志物。作为补充的结果，可以证明测试的五种生物标志物中的四种的浓度显着降低，这表明对炎症系统有强烈的影响。炎症的减少可能是早期报道的干预结果降低心血管发病率和死亡率的积极临床结果背后的机制之一。该研究规模较小，应被视为产生假设，但仍增加了有关目前已知会增加临床影响风险的机制的重要数据，例如降低心血管死亡率、增加心脏功能和改善与健康相关的生活质量评分，如前所述在积极治疗组中得到证实。试验注册 干预研究已在 Clinicaltrials.gov 上注册，标识符为 NCT01443780，并于 2011 年 9 月 30 日注册。但尽管如此，增加了有关目前已知的增加临床效应风险的机制的重要数据，例如降低心血管死亡率、增加心脏功能和更好的与健康相关的生活质量评分，正如之前在积极治疗组中所证明的那样。试验注册 干预研究已在 Clinicaltrials.gov 上注册，标识符为 NCT01443780，并于 2011 年 9 月 30 日注册。但尽管如此，增加了有关目前已知的增加临床效应风险的机制的重要数据，例如降低心血管死亡率、增加心脏功能和更好的与健康相关的生活质量评分，正如之前在积极治疗组中所证明的那样。试验注册 干预研究已在 Clinicaltrials.gov 上注册，标识符为 NCT01443780，并于 2011 年 9 月 30 日注册。