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Published on: May 2, 2025

A prenylated flavan from Broussonetia kazinoki prevents cytokine-induced β-cell death through suppression of nuclear

Ui-Jin Bae1, Da Yeon Lee, Mi-Young Song

  • 1Department of Biochemistry, Research Institute for Endocrine Sciences, and Diabetes Research Center, Chonbuk National University Medical School, Jeonju, Jeonbuk 561–756, Republic of Korea.

Biological & Pharmaceutical Bulletin
|July 2, 2011
PubMed

Insights

Kazinol U protects pancreatic beta cells from damage by blocking the nuclear factor-kappaB (NF-κB) pathway. This natural compound may offer therapeutic benefits for type 1 diabetes by preventing beta cell destruction.

Area of Science:

  • Immunology and Endocrinology
  • Molecular Biology
  • Pharmacology

Background:

  • Cytokine-induced nitric oxide (NO) and reactive oxygen species (ROS) damage pancreatic beta cells.
  • Oxidative stress activates nuclear factor-kappaB (NF-κB), increasing inducible NO synthase (iNOS) expression and beta cell damage.
  • Inhibiting the NF-κB pathway is a potential strategy for protecting beta cells.

Purpose of the Study:

  • To investigate the effects of kazinol U, a prenylated flavan from Broussonetia kazinoki, on NF-κB activation.
  • To determine if kazinol U protects beta cells from cytokine-induced damage.

Main Methods:

  • Treatment of RINm5F cells and islets with kazinol U prior to stimulation with interleukin-1β (IL-1β) and interferon-γ (IFN-γ).
  • Assessed NF-κB activation, including nuclear translocation and DNA binding.
  • Measured IκB kinase (IKK) phosphorylation and IκBα degradation.
  • Quantified nitric oxide (NO), hydrogen peroxide (H2O2) production, and apoptosis.
  • Evaluated insulin secretion from treated islets.

Main Results:

  • Kazinol U completely abolished cytokine-induced cytotoxicity in beta cells.
  • Kazinol U inhibited NF-κB nuclear translocation and DNA binding by suppressing IKK phosphorylation and IκBα degradation.
  • Kazinol U reduced NO and H2O2 production and prevented apoptotic cell death.
  • Insulin secretion from kazinol U-treated islets remained normal in response to glucose.

Conclusions:

  • Kazinol U effectively blocks the NF-κB pathway in pancreatic beta cells.
  • Kazinol U protects beta cells from cytokine-induced damage and preserves insulin secretion.
  • Kazinol U demonstrates therapeutic potential for type 1 diabetes by preventing beta cell destruction.

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