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Journal of Ethnopharmacology 2011-Jan

Taraxacum officinale Weber extracts inhibit LPS-induced oxidative stress and nitric oxide production via the NF-κB modulation in RAW 264.7 cells.

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Chung Mu Park
Ji Young Park
Kyung Hee Noh
Jin Hyuk Shin
Young Sun Song

キーワード

概要

BACKGROUND

The common dandelion (Taraxacum officinale G.H. Weber ex Wiggers, Asteraceae) has been widely used in folklore medicine to treat dyspepsia, heartburn, and spleen and liver disorders.

OBJECTIVE

To compare the antioxidative and anti-inflammatory activities of Taraxacum officinale methanol extract (TOME) and water extract (TOWE) in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells and assess their constitutional differences, including luteolin, chicoric acid, and total phenol content.

METHODS

Antioxidative enzyme activities, nitric oxide (NO) production, and inducible NO synthase (iNOS) and nuclear factor (NF)-κB expression were estimated by biochemical analysis, the Griess reaction, reverse transcription-polymerase chain reaction, western hybridization, and electrophoretic mobility shift assay. High-performance liquid chromatography and the Folin-Ciocalteau method were used to analyze functional phytochemicals and total phenol content.

RESULTS

TOME and TOWE significantly reduced NO production with an IC(50) of 79.9 and 157.5 μg/mL, respectively, without cytotoxicity. Depleted glutathione (GSH) and antioxidative enzyme activities, including superoxide dismutase, catalase, GSH-peroxidase, and GSH-reductase, were restored by dandelion extracts. Both extracts inhibited LPS-stimulated iNOS gene expression and that of its transcription factor, NF-κB, in parallel with nitrite reduction. TOME showed more potent antioxidative and anti-inflammatory capacities than TOWE, which was attributable to its high total phenol, luteolin, and chicoric acid content.

CONCLUSIONS

These results indicate that TOME and TOWE inhibit oxidative stress and inflammatory responses through elevated de novo synthesis of antioxidative enzymes and suppression of iNOS expression by NF-κB inactivation.

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