Methanol extracts of Euphorbia cooperi inhibit the production of inflammatory mediators by inhibiting the activation of c‑Jun N‑terminal kinase and p38 in murine macrophages

Cho,Young‑Chang; Lee,In‑Seon; Seo,Huiyun; Ju,Anna; Youn,Deokkyu; Kim,Younghyun; Choun,Jaehee; Cho,Sayeon

doi:10.3892/mmr.2014.2560

Methanol extracts of Euphorbia cooperi inhibit the production of inflammatory mediators by inhibiting the activation of c‑Jun N‑terminal kinase and p38 in murine macrophages

Authors:
- Young‑Chang Cho
- In‑Seon Lee
- Huiyun Seo
- Anna Ju
- Deokkyu Youn
- Younghyun Kim
- Jaehee Choun
- Sayeon Cho
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Affiliations: College of Pharmacy, Chung‑Ang University, Seoul 156-756, Republic of Korea
Published online on: September 11, 2014 https://doi.org/10.3892/mmr.2014.2560
Pages: 2663-2668

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Abstract

Numerous Euphorbiaceae plants have been used for the treatment of diseases, including liver diseases, asthma and rheumatism. The present study evaluated the effect of methanol extracts from Euphorbia cooperi (MEC), a member of the Euphorbiaceae plant family, on the production of inflammatory cytokines interleukin (IL)‑6 and tumor necrosis factor (TNF)‑α, nitric oxide (NO) as well as the activation of mitogen‑activated protein kinase and nuclear factor (NF)‑κB signaling. Non‑cytotoxic concentrations of MEC significantly reduced the production of NO and IL‑6, but not TNF‑α, in lipopolysaccharide (LPS)‑stimulated RAW 264.7 macrophages. The decreased production of NO by MEC was due to alleviated expression of inducible NO synthase. Reporter assays with cells treated with MEC demonstrated reduced activator protein‑1 (AP-1) activity, while NF‑κB activity was not reduced. Furthermore, the phosphorylation levels of c‑Jun N‑terminal kinase (JNK) and p38 were suppressed by MEC while phosphorylation levels of inhibitor of κB were not reduced by MEC, suggesting that MEC‑mediated inactivation of JNK and p38 is the underlying regulatory mechanism for inflammatory mediators in LPS‑stimulated RAW 264.7 macrophages.

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