Ethyl acetate extract from Angelica Dahuricae Radix inhibits lipopolysaccharide-induced production of nitric oxide, prostaglandin E 2 and tumor necrosis factor-α via mitogen-activated protein kinases and nuclear factor-κB in macrophages
Angelica dahurica (Umbelliferae) has been used to treat headache of common cold, supraorbital neuralgia, painful swelling on the body, nasal stuffiness, leukorrhea and arthralgia due to wind-dampness in Korean traditional medicine. It is also claimed to be effective in the treatment of acne, erythem...
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Published in | Pharmacological research Vol. 55; no. 4; pp. 263 - 270 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Elsevier Ltd
01.04.2007
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Subjects | |
Online Access | Get full text |
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Summary: | Angelica dahurica (Umbelliferae) has been used to treat headache of common cold, supraorbital neuralgia, painful swelling on the body, nasal stuffiness, leukorrhea and arthralgia due to wind-dampness in Korean traditional medicine. It is also claimed to be effective in the treatment of acne, erythema, headache, toothache, sinusitis, colds and flu. The present study focused whether the ethyl acetate extract from Angelica Dahuricae Radix (EAAD) inhibits production of nitric oxide (NO), prostaglandin E
2 (PGE
2) and tumor necrosis factor (TNF)-α, as well as expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs) in lipopolysaccharide (LPS)-stimulated macrophages. EAAD inhibited LPS-induced NO, PGE
2 and TNF-α production as well as expression of iNOS and COX-2 in RAW 264.7 cells. EAAD inhibited LPS-induced TNF-α production in THP-1 cells. Furthermore, EAAD suppressed LPS-induced phosphorylation of p38 MAPK and extracellular-signal regulated kinases 1/2 (ERK1/2), I-κBα degradation, and NF-κB activation in RAW 264.7 cells. These results suggest that EAAD has the inhibitory effects on LPS-induced TNF-α, NO and PGE
2 production, and expression of iNOS and COX-2 in macrophage through blockade in the phosphorylation of MAPKs, following I-κBα degradation and NF-κB activation. |
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ISSN: | 1043-6618 1096-1186 |
DOI: | 10.1016/j.phrs.2006.12.001 |