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Anti-inflammatory effects of trans-1,3-diphenyl-2,3-epoxypropane-1-one mediated by suppression of inflammatory mediators in LPS-stimulated RAW 264.7 macrophages.
Food Chem Toxicol. 2013 Mar; 53:371-5.FC

Abstract

To assess the potential therapeutic properties of trans-1,3-diphenyl-2,3-epoxypropane-1-one (DPEP), its anti-inflammatory effects were investigated in lipopolysaccharide (LPS)-stimulated mouse macrophage (RAW 264.7) cells. DPEP induced dose-dependent reduction of the protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and concomitant reduction in the production of NO and prostaglandin E(2) (PGE(2)). Additionally, DPEP suppressed the production of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6. We investigated the mechanism by which DPEP inhibits NO and PGE(2) by examining the level of nuclear factor-κB (NF-κB) activation within the mitogen-activated protein kinase (MAPK) pathway, which is an inflammation-induced signaling pathway in RAW 264.7 cells. DPEP inhibited LPS-induced phosphorylation of ERK, JNK, and p38. Furthermore, DPEP inhibited the LPS-induced phosphorylation of inhibitor κB (IκB)-α and NF-κB p50. Taken together, the results of this study demonstrate that DPEP inhibits LPS-stimulated inflammation by blocking the NF-κB and MAPK pathways in macrophages.

Authors+Show Affiliations

Marine Bio Research Team, Korea Basic Science Institute (KBSI), Jeju 690-140, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23266270

Citation

Kim, Kil-Nam, et al. "Anti-inflammatory Effects of Trans-1,3-diphenyl-2,3-epoxypropane-1-one Mediated By Suppression of Inflammatory Mediators in LPS-stimulated RAW 264.7 Macrophages." Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association, vol. 53, 2013, pp. 371-5.
Kim KN, Ko YJ, Kang MC, et al. Anti-inflammatory effects of trans-1,3-diphenyl-2,3-epoxypropane-1-one mediated by suppression of inflammatory mediators in LPS-stimulated RAW 264.7 macrophages. Food Chem Toxicol. 2013;53:371-5.
Kim, K. N., Ko, Y. J., Kang, M. C., Yang, H. M., Roh, S. W., Oda, T., Jeon, Y. J., Jung, W. K., Heo, S. J., Yoon, W. J., & Kim, D. (2013). Anti-inflammatory effects of trans-1,3-diphenyl-2,3-epoxypropane-1-one mediated by suppression of inflammatory mediators in LPS-stimulated RAW 264.7 macrophages. Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association, 53, 371-5. https://doi.org/10.1016/j.fct.2012.12.021
Kim KN, et al. Anti-inflammatory Effects of Trans-1,3-diphenyl-2,3-epoxypropane-1-one Mediated By Suppression of Inflammatory Mediators in LPS-stimulated RAW 264.7 Macrophages. Food Chem Toxicol. 2013;53:371-5. PubMed PMID: 23266270.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Anti-inflammatory effects of trans-1,3-diphenyl-2,3-epoxypropane-1-one mediated by suppression of inflammatory mediators in LPS-stimulated RAW 264.7 macrophages. AU - Kim,Kil-Nam, AU - Ko,Yeong-Jong, AU - Kang,Min-Cheol, AU - Yang,Hye-Mi, AU - Roh,Seong Woon, AU - Oda,Tatsuya, AU - Jeon,You-Jin, AU - Jung,Won-Kyo, AU - Heo,Soo-Jin, AU - Yoon,Weon-Jong, AU - Kim,Daekyung, Y1 - 2012/12/21/ PY - 2012/07/27/received PY - 2012/12/12/revised PY - 2012/12/14/accepted PY - 2012/12/26/entrez PY - 2012/12/26/pubmed PY - 2013/8/27/medline SP - 371 EP - 5 JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association JO - Food Chem Toxicol VL - 53 N2 - To assess the potential therapeutic properties of trans-1,3-diphenyl-2,3-epoxypropane-1-one (DPEP), its anti-inflammatory effects were investigated in lipopolysaccharide (LPS)-stimulated mouse macrophage (RAW 264.7) cells. DPEP induced dose-dependent reduction of the protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and concomitant reduction in the production of NO and prostaglandin E(2) (PGE(2)). Additionally, DPEP suppressed the production of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6. We investigated the mechanism by which DPEP inhibits NO and PGE(2) by examining the level of nuclear factor-κB (NF-κB) activation within the mitogen-activated protein kinase (MAPK) pathway, which is an inflammation-induced signaling pathway in RAW 264.7 cells. DPEP inhibited LPS-induced phosphorylation of ERK, JNK, and p38. Furthermore, DPEP inhibited the LPS-induced phosphorylation of inhibitor κB (IκB)-α and NF-κB p50. Taken together, the results of this study demonstrate that DPEP inhibits LPS-stimulated inflammation by blocking the NF-κB and MAPK pathways in macrophages. SN - 1873-6351 UR - https://www.unboundmedicine.com/medline/citation/23266270/Anti_inflammatory_effects_of_trans_13_diphenyl_23_epoxypropane_1_one_mediated_by_suppression_of_inflammatory_mediators_in_LPS_stimulated_RAW_264_7_macrophages_ DB - PRIME DP - Unbound Medicine ER -