Anti-inflammatory Potential of Artemisia capillaris and Its Constituents in LPS-induced RAW264.7 Cells
10.20307/nps.2018.24.3.171
- Author:
Qudeer Ahmed ABDUL
1
;
Su Hui SEONG
;
Bo Ra AHN
;
Md Nurul ISLAM
;
Hyun Ah JUNG
;
Jae Sue CHOI
Author Information
1. Department of Food and Life Science, Pukyong National University, Busan 48513, Republic of Korea. choijs@pknu.ac.kr
- Publication Type:Original Article
- Keywords:
Artemisia capillaris;
Inflammation;
iNOS;
COX-2;
Coumarin;
Flavonoids
- MeSH:
Artemisia;
Blotting, Western;
Dermatitis, Atopic;
Flavonoids;
Inflammation;
Macrophages;
Obesity
- From:Natural Product Sciences
2018;24(3):171-180
- CountryRepublic of Korea
- Language:English
-
Abstract:
Artemisia capillaris has been widely used as an alternative therapy for treating obesity and atopic dermatitis. It has been used as a hepatoprotactant. It is also used for ameliorating inflammatory reactions. Although there are several investigations on other Artemisia species, there is no systematic study describing the role of A. capillaris MeOH extract, its solvent soluble fractions, or derived anti-inflammatory principal components in regulating inflammatory conditions. Therefore, the objective of this study was to elucidate anti-inflammatory mechanisms of A. capillaris. Results revealed that MeOH extract of A. capillaris could decrease LPS-stimulated NO secretion. Of tested fractions, CH₂Cl₂, EtOAc, and n-BuOH strongly inhibited NO release from RAW264.7 cells. Bioactive mediators derived from CH₂Cl₂ and n-BuOH fractions elicited potent anti-inflammatory actions and strikingly abrogated LPS-triggered NO accumulation in RAW264.7 cells. Of particular interest, capillin and isoscopoletin possessed the most potent NO suppressive effects. Western blot analysis validated the molecular mechanism of NO inhibition and showed that capillin and isoscopoletin significantly down-regulated iNOS and COX-2 protein expression. Taken together, our results provide the first evidence that MeOH extract, CH₂Cl₂, EtOAc, and n-BuOH fractions from A. capillaris and its derived lead candidates can potently suppress inflammatory responses in macrophages by hampering NO release and down-regulating iNOS and COX-2 signaling.
