Anti-inflammatory effects of proanthocyanidin-rich red rice extract via suppression of MAPK, AP-1 and NF-κB pathways in Raw 264.7 macrophages.
10.4162/nrp.2016.10.3.251
- Author:
Pornngarm LIMTRAKUL
1
;
Supachai YODKEEREE
;
Pornsiri PITCHAKARN
;
Wanisa PUNFA
Author Information
1. Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand. pornngarm.d@cmu.ac.th
- Publication Type:Original Article
- Keywords:
Cytokines;
inflammation;
lipopolysaccharide;
phenolic;
proanthocyanidin
- MeSH:
Blotting, Western;
Catechin;
Cyclooxygenase 2;
Cytokines;
Enzyme-Linked Immunosorbent Assay;
Inflammation;
Interleukin-6;
Macrophages*;
Necrosis;
NF-kappa B;
Nitric Oxide;
Nitric Oxide Synthase Type II;
p38 Mitogen-Activated Protein Kinases;
Phosphorylation;
Phosphotransferases;
Protein Kinases;
RAW 264.7 Cells;
Transcription Factor AP-1*;
Transcription Factors
- From:Nutrition Research and Practice
2016;10(3):251-258
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND/OBJECTIVES: Several pharmacological properties of red rice extract have been reported including anti-oxidant, anti-tumor, and reduced cancer cell invasion. This study was conducted to evaluate the anti-inflammatory effects of red rice extract on the production of inflammatory mediators in lipopolysaccharide (LPS)-induced Raw 264.7 macrophages. MATERIALS/METHODS: Pro-inflammatory cytokines including tumor necrosis factor-α and interleukin-6 were determined by ELISA and cyclooxygenase-2 and inducible nitric oxide synthase expression was evaluated using western blot analysis. In addition, the signaling pathway controlling the inflammatory cascade such as nuclear factor kappa B (NF-κB), activator proteins-1 (AP-1), and mitogen-activated protein kinase (MAPK) was determined. RESULTS: Our results showed that red rice polar extract fraction (RR-P), but not non-polar extract fraction, inhibited interleukin-6, tumor necrosis factor-α, and nitric oxide production in LPS-induced Raw 264.7 cells. RR-P also reduced the expression of inflammatory enzymes, inducible nitric oxide synthase, and cyclooxygenase-2. In addition, activation of AP-1 and NF-κB transcription factor in the nucleus was abrogated by RR-P. RR-P inhibited the phosphorylation of extracellular signaling-regulated kinase 1/2, c-Jun NH2-terminal kinase, and p38 MAPK signaling responsible for the expression of inflammatory mediators in LPS-stimulated Raw 264.7 cells. Based on chemical analysis, high amounts of proanthocyanidin and catechins were detected in the RR-P fraction. However, only proanthocyanidin reduced NF-κB and AP-1 activation in LPS-activated Raw 264.7 cells. CONCLUSION: These observations suggest that the anti-inflammatory properties of RR-P may stem from the inhibition of pro-inflammatory mediators via suppression of the AP-1, NF-κB, and MAPKs pathways.
