Anti-inflammatory Potential of Artemisia capillaris and Its Constituents in LPS-induced RAW264.7 Cells
2018
Qudeer Ahmed Abdul, Pukyong National University, Busan, Republic of Korea | Seong, S.H., Pukyong National University, Busan, Republic of Korea | Ahn, B.R., Pukyong National University, Busan, Republic of Korea | Md Nurul Islam, Mawlana Bhashani Science and Technology University, Santosh, Tangail, Bangladesh | Jung, H.A., Chonbuk National University, Jeonju, Republic of Korea | Choi, J.S., Pukyong National University, Busan, Republic of Korea
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.
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