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    Title: Berberine suppresses inflammatory agents-induced interleukin-1β and tumor necrosis factor-α productions via the inhibition of IκB degradation in human lung cells
    Authors: 李昌諴(C.H. Lee);陳兆群(Jaw-Chyun Chen);項千芸(Chien-Yun Hsiang);吳世祿(Shih-Lu Wu);吳琇卿(Wu,Hsiu-Chung);侯庭鏞(Tin-Yun Ho)*
    Contributors: 中醫學院中國醫學研究所
    Keywords: Berberine;Interleukin-1β;Tumor necrosis factor-α;Pulmonary inflammation;Inhibitory κB-α
    Date: 2007-09
    Issue Date: 2009-08-24 14:47:23 (UTC+8)
    Abstract: Pulmonary inflammation is a characteristic of many lung diseases. Increased levels of pro-inflammatory cytokines, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), have been correlated with lung inflammation. In this study, we demonstrated that various inflammatory agents, including lipopolysaccharide, 12-o-tetradecanoylphorbol-13-acetate, hydrogen peroxide, okadaic acid and ceramide, were able to induce IL-1β and TNF-α productions in human lung epithelial cells (A-549), fibroblasts (HFL1), and lymphoma cells (U-937). Berberine, the protoberberine alkaloid widely distributed in the plant kingdom, was capable of suppressing inflammatory agents-induced cytokine production in lung cells. Inhibition of cytokine production by berberine was dose-dependent and cell type-independent. Moreover, the suppression of berberine on the cytokine production resulted from the inhibition of inhibitory κB-α phosphorylation and degradation. In conclusion, our findings suggested the potential role of berberine in the treatment of pulmonary inflammation.
    Relation: PHARMACOLOGICAL RESEARCH 56(3)193~201
    Appears in Collections:[Graduate Institute of Chinese Medical Science] Journal articles

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