Berberine suppresses inflammatory agents-induced interleukin-1beta and tumor necrosis factor-alpha productions via the inhibition of IkappaB degradation in human lung cells.
Pulmonary inflammation is a characteristic of many lung diseases. Increased levels of pro-inflammatory cytokines, such as interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), 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-1beta and TNF-alpha 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 kappaB-alpha phosphorylation and degradation. In conclusion, our findings suggested the potential role of berberine in the treatment of pulmonary inflammation.
Lee
Chang-Hsien
CH
Molecular Biology Laboratory, Graduate Institute of Chinese Medical Science, China Medical University, 91 Hsueh-Shih Road, Taichung 40402, Taiwan.
Chen
Jaw-Chyun
JC
Hsiang
Chien-Yun
CY
Wu
Shih-Lu
SL
Wu
Hsiu-Ching
HC
Ho
Tin-Yun
TY
D000470:Alkaloids / Q000633:toxicity; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000633:toxicity; D053119:Benzophenanthridines / Q000633:toxicity; D001599:Berberine / Q000494:pharmacology* / Q000633:toxicity; D002470:Cell Survival / Q000187:drug effects; D002518:Ceramides / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D020672:I-kappa B Proteins / Q000378:metabolism*; D007249:Inflammation / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D053583:Interleukin-1beta / Q000378:metabolism*; D007546:Isoquinolines / Q000633:toxicity; D008070:Lipopolysaccharides / Q000494:pharmacology; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D000072000:NF-KappaB Inhibitor alpha; D019319:Okadaic Acid / Q000494:pharmacology; D010766:Phosphorylation; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D020298:U937 Cells
D000470:Alkaloids; D000893:Anti-Inflammatory Agents; D053119:Benzophenanthridines; D002518:Ceramides; D020672:I-kappa B Proteins; D053583:Interleukin-1beta; D007546:Isoquinolines; D008070:Lipopolysaccharides; C000606204:NFKBIA protein, human; D014409:Tumor Necrosis Factor-alpha; D001599:Berberine; D000072000:NF-KappaB Inhibitor alpha; D019319:Okadaic Acid; C005705:sanguinarine; D006861:Hydrogen Peroxide; C016299:chelerythrine; D013755:Tetradecanoylphorbol Acetate