- Author:
Kang Pa LEE
1
;
Giftania Wardani SUDJARWO
;
Ji Su KIM
;
Septrianto DIRGANTARA
;
Won Jai MAENG
;
Heeok HONG
Author Information
- Publication Type:In Vitro ; Original Article
- Keywords: Areca catechu; anti-inflammation; lipopolysaccharide (LPS); carrageenan; RAW 264.7 cell; paw edema
- MeSH: Areca*; Blotting, Western; Carrageenan; Cyclooxygenase 2; Down-Regulation; Edema; Ethanol; Fruit; Herbal Medicine; Humans; Indonesia; Inflammation; NF-kappa B; Nitric Oxide; Nitric Oxide Synthase Type II
- From:Nutrition Research and Practice 2014;8(3):267-271
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/OBJECTIVES: Overproduction of nitric oxide (NO) by the inducible nitric oxide synthase (iNOS) enzyme can cause inflammation. Cyclooxygenase-2 (COX-2) is also involved in the inflammatory response through regulation of nuclear factor-kappa B (NF-kappaB). Areca catechu is one of the known fruit plants of the Palmaceae family. It has been used for a long time as a source of herbal medicine in Indonesia. In this study, we explored the effect of Indonesian Areca catechu leaf ethanol extract (ACE) in lipopolysaccharide (LPS)-induced inflammation and carrageenan-induced paw edema models. Recently, this natural extract has been in the spotlight because of its efficacy and limited or no toxic side effects. However, the mechanism underlying its anti-inflammatory effect remains to be elucidated. MATERIALS/METHODS: We measured NO production by using the Griess reagent, and determined the expression levels of inflammation-related proteins, such as iNOS, COX2, and NF-kappaB, by western blot. To confirm the effect of ACE in vivo, we used the carrageenan-induced paw edema model. RESULTS: Compared to untreated cells, LPS-stimulated RAW 264.7 cells treated with ACE showed reduced NO generation and reduced iNOS and COX-2 expression. We found that the acute inflammatory response was significantly reduced by ACE in the carrageenan-induced paw edema model. CONCLUSION: Taken together, these results suggest that ACE can inhibit inflammation and modulate NO generation via downregulation of iNOS levels and NF-kappaB signaling in vitro and in vivo. ACE may have a potential medical benefit as an anti-inflammation agent.