Conjugated linoleic acid attenuates the production and gene expression of proinflammatory cytokines in weaned pigs challenged with lipopolysaccharide
Conjugated linoleic acid attenuates the production and gene expression of proinflammatory cytokines in weaned pigs challenged with lipopolysaccharide
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DOI：
10.1093/jn/135.2.239
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发表时间：
2005-02-01
影响因子：
4.2
通讯作者：
Xing, JJ
中科院分区：
文献类型：
--
作者：
Lai, CH;Yin, JD;Xing, JJ
我们研究了共轭亚油酸（CLA）在炎症激发的断奶仔猪和体外培养的外周血单个核细胞（PBMC）中的抗炎作用。为了检验炎症反应可以通过膳食CLA补充剂减弱的假设，我们使用了猪注射脂多糖（LPS）的急性炎症模型。在日粮中添加2%豆油或2%共轭亚油酸14 d后，每个日粮组中各有一半的猪用LPS攻击。膳食CLA减轻了生长抑制并防止了促炎细胞因子的产生和mRNA表达的升高[即，白细胞介素（IL）-6和肿瘤坏死因子（TNF）-α]。CLA可增强脾脏和胸腺中白细胞介素-10（IL-10）和过氧化物酶体增殖物激活受体-γ（PPARgamma）的表达。为了进一步阐明CLA对细胞因子谱的抑制作用和作用机制（即，IL-1 β、IL-6和TNF-α），从断奶猪中分离PBMC，并在含有顺式-9，反式-11（9 c，11 t）CLA和反式-10，顺式-12（10 t，12 c）CLA的培养基中培养。在培养的PBMC中，每种CLA异构体均抑制IL-1 β、IL-6和TNF-α的产生和表达，并增强PPARgamma的活化和基因表达。在分子水平上，CLA对IL-10、IL-6和TNF-α的抑制作用主要归因于10 t，12 c-CLA，并且CLA的抗炎性质至少部分地通过PPAR-γ依赖性机制介导。
We investigated the anti-inflammatory role of conjugated linoleic acid (CLA) in inflammation-challenged weaned pigs and in in vitro cultured peripheral blood mononuclear cells (PBMCs). To test the hypothesis that inflammation responses can be attenuated by dietary CLA supplementation, we used an acute inflammation model in which pigs were injected with lipopolysaccharide (LPS). After 14 d of dietary supplementation with either 2% soybean oil or 2% CLA, half of the pigs in each diet group were challenged with LPS. Dietary CLA alleviated growth depression and prevented the elevations in production and mRNA expression of proinflammatory cytokines [i.e., interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha] induced by the LPS challenge. CLA enhanced the expression of interleukin-10 (IL-10) and peroxisome proliferator-activated receptor-gamma (PPARgamma) in spleen and thymus. To further elucidate the inhibitory effects and the mechanism of action of CLA on cytokine profiles (i.e., IL-1beta, IL-6, and TNF-alpha), PBMCs were isolated from weaned pigs and cultured in media containing cis-9, trans-11 (9c,11t) CLA and trans-10, cis-12 (10t,12c) CLA. Each CLA isomer suppressed the production and expression of IL-1beta, IL-6, and TNF-alpha, and enhanced PPARgamma activation and gene expression in cultured PBMCs. At the molecular level, the inhibitory actions of CLA on IL-10, IL-6, and TNF-alpha are attributable mainly to 10t,12c-CLA and the anti-inflammatory properties of CLA are mediated, at least in part, through a PPAR-gamma-dependent mechanism.