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Roxithromycin inhibits transforming growth factor-beta production by cultured human mesangial cells

Hideaki Yamabe1, Michiko Shimada, Mitsuaki Kaizuka

  • 1The Second Department of Internal Medicine, Hirosaki University School of Medicine, Hirosaki, Japan. yamabe@cc.hirosaki-u.ac.jp

Nephrology (Carlton, Vic.)
|January 4, 2007
PubMed
Abstract

Insights

Roxithromycin (ROX) inhibits transforming growth factor-beta (TGF-beta) production in human mesangial cells, potentially treating glomerulosclerosis. This macrolide antibiotic may offer therapeutic benefits for kidney injury by targeting TGF-beta pathways.

Area of Science:

  • Nephrology
  • Pharmacology
  • Cell Biology

Background:

  • Transforming growth factor-beta (TGF-beta) is implicated in renal injury progression.
  • Few effective inhibitors of TGF-beta are known.
  • Roxithromycin (ROX), a macrolide antibiotic, exhibits anti-inflammatory and tissue reparative effects, but its mechanisms are unclear.

Purpose of the Study:

  • To investigate the effect of Roxithromycin (ROX) on TGF-beta and type IV collagen production in cultured human mesangial cells (HMC).
  • To explore the potential role of NF-kappaB signaling in ROX's mechanism of action.

Main Methods:

  • Human mesangial cells (HMC) were treated with varying concentrations of ROX.
  • TGF-beta and type IV collagen levels were measured using enzyme-linked immunoassay.
  • TGF-beta mRNA expression was quantified, and the impact of ROX on thrombin-stimulated signaling pathways (tyrosine kinase, MAP kinase, NF-kappaB) was assessed.

Main Results:

  • ROX dose-dependently inhibited TGF-beta production and mRNA expression in HMC without causing cell toxicity.
  • ROX significantly suppressed thrombin-induced TGF-beta and type IV collagen production.
  • ROX inhibited thrombin-induced NF-kappaB activation but not tyrosine kinase or MAP kinase.

Conclusions:

  • Roxithromycin inhibits TGF-beta production in HMC, likely through NF-kappaB pathway modulation.
  • ROX demonstrates potential as a therapeutic agent for treating glomerulosclerosis and related kidney diseases.

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