Taraxacum officinale Weber extracts inhibit LPS-induced oxidative stress and nitric oxide production via the NF-κB modulation in RAW 264.7 cells
2011
Park, Chung Mu | Park, Ji Young | Noh, Kyung Hee | Shin, Jin Hyuk | Song, Yŏng-sŏn
ETHNOPHARMACOLOGICAL RELEVANCE: 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. AIM OF THE STUDY: 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. MATERIALS AND 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 IC₅₀ of 79.9 and 157.5μg/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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