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Protective Role of Nuclear Factor E2-Related Factor 2 against Acute Oxidative Stress-Induced Pancreatic β -Cell

Jingqi Fu1, Hongzhi Zheng2, Huihui Wang1

  • 1Program of Environmental Toxicology, School of Public Health, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning 110122, China.

Oxidative Medicine and Cellular Longevity
|May 8, 2015
PubMed

Insights

Nuclear factor E2-related factor 2 (NRF2) protects pancreatic beta cells from oxidative stress. Silencing NRF2 worsens damage, while activators offer protection, suggesting NRF2

Area of Science:

  • * Endocrinology and Metabolism
  • * Cellular Biology and Oxidative Stress

Background:

  • * Oxidative stress is a key factor in pancreatic beta-cell dysfunction in both type 1 and type 2 diabetes.
  • * Nuclear factor E2-related factor 2 (NRF2) is a crucial regulator of cellular antioxidant responses.

Purpose of the Study:

  • * To investigate the role of NRF2 in protecting pancreatic beta-cells against oxidative stress and its implications in diabetes pathogenesis.
  • * To examine the effects of NRF2 activators and knockdown on beta-cell response to oxidative stressors.

Main Methods:

  • * Utilized MIN6 beta-cells with stable Nrf2 knockdown (Nrf2-KD) and Nrf2-knockout mouse islets.
  • * Exposed cells and islets to oxidative stressors like hydrogen peroxide (H2O2) and S-nitroso-N-acetylpenicillamine.
  • * Assessed cell viability, ATP content, islet morphology, and apoptotic biomarkers.
  • * Evaluated the protective effects of NRF2 activators (CDDO-Im, DMF, tBHQ).

Main Results:

  • * Nrf2 knockdown cells and knockout islets showed reduced antioxidant enzyme levels and increased sensitivity to oxidative damage.
  • * Oxidative stressors caused concentration- and time-dependent cell damage in control cells and wild-type islets.
  • * NRF2 activators protected MIN6 cells from H2O2-induced damage.
  • * Persistent NRF2 activation blunted glucose-triggered reactive oxygen species (ROS) signaling and glucose-stimulated insulin secretion (GSIS).

Conclusions:

  • * NRF2 plays a protective role against oxidative stress in pancreatic beta-cells.
  • * NRF2 modulation influences beta-cell response to oxidative damage and may have distinct roles in different diabetes stages.
  • * NRF2 activators show potential for protecting beta-cells, but their impact on GSIS needs consideration.

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