In situ generation, metabolism and immunomodulatory signaling actions of nitro-conjugated linoleic acid in a murine model of inflammation

Conjugated linoleic acid (CLA) is a prime substrate for intra-gastric nitration giving rise to the formation of nitroconjugated 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 resu...

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Tác giả chính: Villacorta, Luis (author)
Tác giả khác: Minarrieta, Lucia (author), Salvatore, Sonia R. (author), Khoo, Nicholas K. (author), Rom, Oren (author), Gao, Zhen (author), Berman, Rebecca C. (author), Jobbagy, Soma (author), Li, Lihua (author), Woodcock, Steven R. (author), Chen, Y. Eugene (author), Freeman, Bruce A. (author), Ferreira, Ana M. (author), Schopfer, Francisco J. (author), Vitturi, Dario A. (author)
Định dạng: article
Ngôn ngữ:Tiếng Anh
Được phát hành: 2018
Những chủ đề:
Truy cập trực tuyến:https://hdl.handle.net/20.500.12008/50838
Các nhãn: Thêm thẻ
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Tóm tắt:Conjugated linoleic acid (CLA) is a prime substrate for intra-gastric nitration giving rise to the formation of nitroconjugated 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.