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.
Molecular Biology Laboratory, Graduate Institute of Chinese Medical Science, China Medical University, 91 Hsueh-Shih Road, Taichung 40402, Taiwan.
Chang-Hsien
CH
Lee
Jaw-Chyun
JC
Chen
Chien-Yun
CY
Hsiang
Shih-Lu
SL
Wu
Hsiu-Ching
HC
Wu
Tin-Yun
TY
Ho
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