Pediatrics and neonatology · 2008
Effect of the Chinese herb extract osthol on IL-4-induced eotaxin expression in BEAS-2B cells.
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Chiu Pu-Rong, Lee Wei-Te, Chu Yu-Te, Lee Min-Sheng, Jong Yuh-Jyh, Hung Chih-Hsing
Аннотация
BACKGROUND: Asthma is an allergic inflammatory disease of the airways. The interaction between bronchial epithelial cells and eosinophils is an important feature of an asthma attack. Eotaxin, an eosinophil-specific C-C chemokine, is a potent chemoattractant involved in the mobilization of eosinophils into the airway after allergic stimulation. Cnidii monnieri fructus, the dried fruit of Cnidium monnieri Cusson, has been used as an antipruritogenic agent in ancient China. OsthoL is the major component of Cnidii monnieri fructus extract. We investigated the ability of osthol to regulate cytokine-induced eotaxin expression in the human bronchial epithelial cell line BEAS-2B.
METHODS: BEAS-2B cells were pretreated with osthol at different concentrations (0.1-10 microM), and then stimulated with interleukin (IL)-4 alone, or in combination with tumor necrosis factor (TNF)-alpha. Eotaxin levels were determined by real-time reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. STAT6 (signal transducer and activator of transcription 6) and MAPK (mitogen-activated protein kinase) expressions were evaluated by Western blotting, to detect possible intracellular signal transduction.
RESULTS: IL-4 and TNF-alpha significantly induced eotaxin expression in BEAS-2B cells. Expression of eotaxin was suppressed by osthol (0.1-10 microM) in a dose-dependent manner. Osthol did not suppress IL-4-induced p38, ERK or JNK expression. Osthol did suppress IL-4-induced STAT6 in a dose-dependent manner.
CONCLUSION: Osthol suppressed IL-4-induced eotaxin in BEAS-2B cells via inhibition of STAT6 expression. This data suggest that osthol might have potential for treating allergic airway inflammation.
METHODS: BEAS-2B cells were pretreated with osthol at different concentrations (0.1-10 microM), and then stimulated with interleukin (IL)-4 alone, or in combination with tumor necrosis factor (TNF)-alpha. Eotaxin levels were determined by real-time reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. STAT6 (signal transducer and activator of transcription 6) and MAPK (mitogen-activated protein kinase) expressions were evaluated by Western blotting, to detect possible intracellular signal transduction.
RESULTS: IL-4 and TNF-alpha significantly induced eotaxin expression in BEAS-2B cells. Expression of eotaxin was suppressed by osthol (0.1-10 microM) in a dose-dependent manner. Osthol did not suppress IL-4-induced p38, ERK or JNK expression. Osthol did suppress IL-4-induced STAT6 in a dose-dependent manner.
CONCLUSION: Osthol suppressed IL-4-induced eotaxin in BEAS-2B cells via inhibition of STAT6 expression. This data suggest that osthol might have potential for treating allergic airway inflammation.