Radicicol inhibits iNOS expression in cytokine-stimulated pancreatic beta cells

Cha Kyung Youn, Seon Joo Park, Mei Hong Li, Min Young Lee, Kun Yeong Lee, Man Jin Cha, Ok Hyeun Kim, Ho Jin You, In Youp Chang, Sang Pil Y. Oon, Young Jin Jeon

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


Here, we show that radicicol, a fungal antibiotic, resulted in marked inhibition of inducible nitric oxide synthase (iNOS) transcription by the pancreatic beta cell line MIN6N8a in response to cytokine mixture (CM: TNF-α, IFN-γ, and IL-1 β). Treatment of MIN6N8a cells with radicicol inhibited CM-stimulated activation of NF-κ B/Rel, which plays a critical role in iNOS transcription, in a dose-related manner. Nitrite production in the presence of PD98059, a specific inhibitor of the extracellular signal-regulated protein kinase-1 and 2 (ERK1/2) pathway, was dramatically diminished, suggesting that the ERK1/2 pathway is involved in CM-induced iNOS expression. In contrast, SB203580, a specific inhibitor of p38, had no effect on nitrite generation. Collectively, this series of experiments indicates that radicicol inhibits iNOS gene expression by blocking ERK1/2 signaling. Due to the critical role that NO release plays in mediating destruction of pancreatic beta cells, the inhibitory effects of radicicol on iNOS expression suggest that radicicol may represent a useful anti-diabetic activity.

Original languageEnglish (US)
Pages (from-to)315-320
Number of pages6
JournalKorean Journal of Physiology and Pharmacology
Issue number4
StatePublished - Aug 2013


  • ERK1/2
  • INOS
  • NO
  • β cells


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