Berberine suppresses inflammatory agents-induced interleukin-1beta and tumor necrosis factor-alpha productions via the inhibition of IkappaB degradation in human lung cells

Pharmacol Res. 2007 Sep;56(3):193-201. doi: 10.1016/j.phrs.2007.06.003. Epub 2007 Jun 21.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alkaloids / toxicity
  • Anti-Inflammatory Agents / pharmacology*
  • Anti-Inflammatory Agents / toxicity
  • Benzophenanthridines / toxicity
  • Berberine / pharmacology*
  • Berberine / toxicity
  • Cell Survival / drug effects
  • Ceramides / pharmacology
  • Dose-Response Relationship, Drug
  • Epithelial Cells / drug effects
  • Epithelial Cells / metabolism
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism
  • Humans
  • Hydrogen Peroxide / pharmacology
  • I-kappa B Proteins / metabolism*
  • Inflammation / metabolism
  • Inflammation / pathology
  • Inflammation / prevention & control*
  • Interleukin-1beta / metabolism*
  • Isoquinolines / toxicity
  • Lipopolysaccharides / pharmacology
  • Lung / drug effects*
  • Lung / metabolism
  • Lung / pathology
  • NF-KappaB Inhibitor alpha
  • Okadaic Acid / pharmacology
  • Phosphorylation
  • Tetradecanoylphorbol Acetate / pharmacology
  • Tumor Necrosis Factor-alpha / metabolism*
  • U937 Cells

Substances

  • Alkaloids
  • Anti-Inflammatory Agents
  • Benzophenanthridines
  • Ceramides
  • I-kappa B Proteins
  • Interleukin-1beta
  • Isoquinolines
  • Lipopolysaccharides
  • NFKBIA protein, human
  • Tumor Necrosis Factor-alpha
  • Berberine
  • NF-KappaB Inhibitor alpha
  • Okadaic Acid
  • sanguinarine
  • Hydrogen Peroxide
  • chelerythrine
  • Tetradecanoylphorbol Acetate