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Oxidative stress is implicated in the pathogenesis of pancreatic  β -cell dysfunction that occurs in both type 1 and type 2 diabetes. Nuclear factor E2-related factor 2 (NRF2) is a master regulator in the cellular adaptive response to oxidative stress. The present study found that MIN6  β -cells with stable knockdown of  Nrf2  ( Nrf2 -KD) and islets isolated from  Nrf2 -knockout mice expressed substantially reduced levels of antioxidant enzymes in response to a variety of stressors. In scramble MIN6 cells or wild-type islets, acute exposure to oxidative stressors, including hydrogen peroxide (H 2 O 2 ) and S-nitroso-N-acetylpenicillamine, resulted in cell damage as determined by decrease in cell viability, reduced ATP content, morphology changes of islets, and/or alterations of apoptotic biomarkers in a concentration- and/or time-dependent manner. In contrast, silencing of  Nrf2  sensitized MIN6 cells or islets to the damage. In addition, pretreatment of MIN6  β -cells with NRF2 activators, including CDDO-Im, dimethyl fumarate (DMF), and  tert -butylhydroquinone (tBHQ), protected the cells from high levels of H 2 O 2 -induced cell damage. Given that reactive oxygen species (ROS) are involved in regulating glucose-stimulated insulin secretion (GSIS) and persistent activation of NRF2 blunts glucose-triggered ROS signaling and GSIS, the present study highlights the distinct roles that NRF2 may play in pancreatic  β -cell dysfunction that occurs in different stages of diabetes.

Protective Role of Nuclear Factor E2-Related Factor 2 against Acute Oxidative Stress-Induced Pancreaticβ-Cell Damage