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[Oxidative stress induces apoptosis via NF-kappaB-iNOS-nitric oxide pathway in pancreatic beta-cells]

Yan-ping Wang1, Xiao-dong Pan, Su-yuan Jiang

  • 1Fujian Institute of Endocrinology, Union Hospital, Fujian Medical University, Fuzhou 350001, China.

Zhongguo Ying Yong Sheng Li Xue Za Zhi = Zhongguo Yingyong Shenglixue Zazhi = Chinese Journal of Applied Physiology
|December 31, 2010
PubMed
Abstract

Insights

Tert-butyl hydroperoxide (t-BHP) induces apoptosis in pancreatic beta-cells via the NF-kappaB-iNOS-nitric oxide pathway. This mechanism involves increased nitric oxide production and cell death, which can be mitigated by specific inhibitors.

Area of Science:

  • Cell biology
  • Molecular biology
  • Biochemistry

Context:

  • Murine MIN6 pancreatic beta-cells are a model system for studying beta-cell function and dysfunction.
  • Oxidative stress, induced by agents like tert-butyl hydroperoxide (t-BHP), is implicated in beta-cell damage and the pathogenesis of diabetes.
  • Understanding the molecular mechanisms of t-BHP-induced apoptosis is crucial for developing therapeutic strategies.

Purpose:

  • To elucidate the mechanism by which tert-butyl hydroperoxide (t-BHP) induces apoptosis in murine MIN6 pancreatic beta-cells.
  • To investigate the role of the NF-kappaB-iNOS-nitric oxide signaling pathway in t-BHP-mediated beta-cell death.

Summary:

  • Exposure of MIN6 cells to t-BHP significantly reduced cell viability and increased apoptosis.
  • t-BHP elevated cytoplasmic inducible nitric oxide synthase (iNOS) protein and nitrite levels, alongside nuclear NF-kappaBp65 fragmentation.
  • Inhibitors L-NAME and N-Acetyl-l-cysteine (NAC) attenuated t-BHP-induced nitrite production and apoptosis, confirming the pathway's involvement.

Impact:

  • Identifies the NF-kappaB-iNOS-nitric oxide pathway as a key mediator of t-BHP-induced apoptosis in pancreatic beta-cells.
  • Provides insights into the molecular basis of oxidative stress-induced beta-cell damage.
  • Suggests potential therapeutic targets for protecting beta-cells from oxidative injury in conditions like diabetes.

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