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剧烈运动可减少小鼠脂多糖应答产生的肿瘤坏死因子-α。

Exhaustive exercise reduces tumor necrosis factor-alpha production in response to lipopolysaccharide in mice.

机构信息

Department of Health and Sports Science, Kawasaki University of Medical Welfare, Kurashiki, Japan.

出版信息

Neuroimmunomodulation. 2010;17(4):279-86. doi: 10.1159/000290044. Epub 2010 Mar 5.

DOI:10.1159/000290044
PMID:20203534
Abstract

OBJECTIVE

Stressful exercise reduces the plasma pro-inflammatory cytokine concentration in response to lipopolysaccharide (LPS). The aim of this study was to clarify the mechanism of exhaustive exercise-induced suppression of the plasma tumor necrosis factor (TNF)-alpha concentration in response to LPS.

METHODS

Male C3H/HeN mice (n = 66) were randomized to treadmill running to exhaustion (Ex) or a sedentary (Non-Ex) condition. Monocytes and splenic macrophages were collected from some animals, and other animals were injected with LPS (1 mg/kg) immediately after the exercise. The liver, lung and spleen tissues in the mice were removed 30 min after the LPS injection for determination of TNF-alpha mRNA expression. Blood and tissue samples were collected for determination of TNF-alpha and TNF receptors (TNFR) 1 h after the LPS injection.

RESULTS

Although there was a significant suppression in LPS-induced plasma TNF-alpha in the Ex mice when compared to the Non-Ex mice (p < 0.01), soluble TNFR in plasma was not affected by the exercise. There was no change in cell-surface expression of Toll-like receptor 4 (TLR4) and in LPS-induced TNF-alpha mRNA expression and TNFR content in tissues between the Ex and Non-Ex groups. Interestingly, TNF-alpha contents in the liver, lung and spleen of the Ex mice were significantly lower than those of the Non-Ex group (p < 0.01, p < 0.01 and p < 0.05, respectively).

CONCLUSION

These data suggest that exhaustive exercise-induced suppression of the plasma TNF-alpha concentration despite LPS stimulation might depend on translation of TNF-alpha in tissues.

摘要

目的

应激运动可降低脂多糖(LPS)刺激后血浆促炎细胞因子浓度。本研究旨在阐明运动性疲劳抑制 LPS 刺激后血浆肿瘤坏死因子(TNF)-α浓度的机制。

方法

雄性 C3H/HeN 小鼠(n=66)被随机分为跑步机运动至力竭(Ex)或安静(Non-Ex)组。从一些动物中收集单核细胞和脾巨噬细胞,其他动物在运动后立即注射 LPS(1mg/kg)。LPS 注射后 30 分钟,取出小鼠的肝、肺和脾组织,测定 TNF-α mRNA 表达。LPS 注射后 1 小时,采集血液和组织样本,测定 TNF-α和 TNF 受体(TNFR)1。

结果

与 Non-Ex 组相比,Ex 组 LPS 诱导的血浆 TNF-α显著降低(p<0.01),但血浆可溶性 TNFR 不受运动影响。Ex 组和 Non-Ex 组之间 TLR4 细胞表面表达、LPS 诱导的 TNF-α mRNA 表达和组织中 TNFR 含量均无变化。有趣的是,Ex 组小鼠肝、肺和脾中的 TNF-α含量明显低于 Non-Ex 组(p<0.01、p<0.01 和 p<0.05)。

结论

这些数据表明,尽管 LPS 刺激,运动性疲劳仍可抑制血浆 TNF-α浓度,这可能依赖于组织中 TNF-α的翻译。

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