Effects of DHMEQ, a novel nuclear factor-κB inhibitor, on beta cell dysfunction in INS-1 cells

Yoshifumi Saisho, Hiroshi Hirose, Chihiro Horimai, Kiichi Miyashita, Izumi Takei, Kazuo Umezawa, Hiroshi Itoh

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)


Aims: Recent studies suggest that nuclear factor-κB (NF-κB) activation has an important role in leading to beta cell dysfunction in both type 1 and type 2 diabetes. In this study we tested this hypothesis by investigating the effects of dehydroxymethylepoxyquinomicin (DHMEQ), a novel NF-κB inhibitor, on tumor necrosis factor-α (TNF-α)-induced beta cell dysfunction. Methods: INS-1 cells were incubated with TNF-α and with or without DHMEQ for 24 hours. Glucose-stimulated insulin secretion, cell viability, mRNA expression and NF-?̂B activation were investigated. Results: DHMEQ suppressed TNF-α-induced NF-κB activation and partially ameliorated glucose-stimulated insulin secretion in a dose-dependent manner. DHMEQ also partially ameliorated decreased cell viability and insulin mRNA level induced by TNF-α. Conclusion: DHMEQ suppressed NF-κB activation and ameliorated beta cell dysfunction induced by TNF-α. Inhibition of activated NF-κB in beta cells may be important to ameliorate beta cell dysfunction in diabetes.

Original languageEnglish
Pages (from-to)433-438
Number of pages6
JournalEndocrine journal
Issue number2
Publication statusPublished - 2008


  • Cell viability
  • Dehydroxymethylepoxyquinomicin
  • Glucose-stimulated insulin secretion
  • INS-1 cells
  • Nuclear factor-κB
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology


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