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首页> 外文期刊>Redox Biology >In situ generation, metabolism and immunomodulatory signaling actions of nitro-conjugated linoleic acid in a murine model of inflammation
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In situ generation, metabolism and immunomodulatory signaling actions of nitro-conjugated linoleic acid in a murine model of inflammation

机译：硝基共轭亚油酸在小鼠炎症模型中的原位产生，代谢和免疫调节信号转导作用

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摘要

Conjugated linoleic acid (CLA) is a prime substrate for intra-gastric nitration giving rise to the formation of nitro-conjugated linoleic acid (NO2-CLA). Herein, NO2-CLA generation is demonstrated within the context of acute inflammatory responses both in vitro and in vivo . Macrophage activation resulted in dose- and time-dependent CLA nitration and also in the production of secondary electrophilic and non-electrophilic derivatives. Both exogenous NO2-CLA as well as that generated in situ , attenuated NF-κB-dependent gene expression, decreased pro-inflammatory cytokine production and up-regulated Nrf2-regulated proteins. Importantly, both CLA nitration and the corresponding downstream anti-inflammatory actions of NO2-CLA were recapitulated in a mouse peritonitis model where NO2-CLA administration decreased pro-inflammatory cytokines and inhibited leukocyte recruitment. Taken together, our results demonstrate that the formation of NO2-CLA has the potential to function as an adaptive response capable of not only modulating inflammation amplitude but also protecting neighboring tissues via the expression of Nrf2-dependent genes.
机译：共轭亚油酸（CLA）是胃内硝化的主要底物，导致形成硝基共轭亚油酸（NO 2 -CLA）。本文在体外和体内急性炎症反应的背景下证实了NO 2 -CLA的产生。巨噬细胞活化导致剂量依赖性和时间依赖性的CLA硝化作用，并导致产生第二亲电和非亲电衍生物。外源NO 2 -CLA以及原位生成的NO 2 -CLA均减弱了NF-κB依赖性基因的表达，降低了促炎细胞因子的产生，并上调了Nrf2调节的蛋白。重要的是，在小鼠腹膜炎模型中概括了CLA硝化作用和相应的NO 2 -CLA下游抗炎作用，其中NO 2 -CLA给药降低了促炎细胞因子并抑制白细胞募集。综上所述，我们的结果表明，NO 2 -CLA的形成具有潜在的适应性反应能力，不仅可以调节炎症幅度，而且还可以通过表达Nrf2依赖性基因来保护邻近组织。 。

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