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The protective effects of Berberine and Hesperidin on inflammatory factor-stimulating cardiac fibroblasts

X-H Yu1, Y-F Wang, F-Y Dai

  • 1Cardiovascular Medicine, Beijing University of Chinese Medicine, Beijing, China. dr_pingli@126.com.

European Review for Medical and Pharmacological Sciences
|July 13, 2019
PubMed

Insights

Berberine and Hesperidin reduce inflammatory cytokine secretion and cardiac fibroblast proliferation by modulating the Notch1 signaling pathway. These natural compounds offer potential therapeutic benefits for cardiovascular diseases by improving collagen synthesis.

Area of Science:

  • Cardiovascular Pharmacology
  • Cell Biology
  • Molecular Medicine

Background:

  • Berberine and Hesperidin demonstrate known cardiovascular benefits, but their underlying mechanisms are not fully understood.
  • Cardiac fibroblasts play a crucial role in cardiovascular disease pathogenesis through inflammatory cytokine secretion, proliferation, differentiation, and collagen synthesis.
  • Transforming growth factor-β1 (TGF-β1) is a key mediator in cardiac fibroblast activation and extracellular matrix remodeling.

Purpose of the Study:

  • To investigate the effects of Berberine and Hesperidin on TGF-β1-stimulated cardiac fibroblasts.
  • To elucidate the role of the Notch1 signaling pathway in the protective actions of Berberine and Hesperidin.

Main Methods:

  • Primary neonatal rat cardiac fibroblasts were stimulated with TGF-β1.
  • Cells were treated with varying concentrations of Berberine or Hesperidin.
  • Notch1 signaling was inhibited using a γ-secretase inhibitor (DAPT) to assess its role.

Main Results:

  • Berberine and Hesperidin reduced inflammatory cytokine (IL-1β) secretion and TGF-β1 levels.
  • Both compounds decreased α-SMA expression and cell viability in a dose-dependent manner, without affecting apoptosis.
  • Berberine and Hesperidin inhibited MMP-1 and MMP-9 expression, and blocking Notch1 signaling reversed these protective effects.

Conclusions:

  • Berberine and Hesperidin mitigate TGF-β1-induced inflammatory cytokine secretion, fibroblast differentiation, and proliferation.
  • These compounds enhance collagen synthesis in cardiac fibroblasts.
  • The protective effects are mediated through the Notch1 signaling pathway.
Abstract

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