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Anthocyanins from Chinese Bayberry Extract Activate Transcription Factor Nrf2 in β Cells and Negatively Regulate Oxidative Stress-Induced Autophagy

2013; American Chemical Society; Volume: 61; Issue: 37 Linguagem: Inglês

10.1021/jf4012399

1520-5118

Bo Zhang, Miranbieke Buya, Wenjie Qin, Chongde Sun, Haolei Cai, Qiuping Xie, Bing Xu, Yulian Wu,

Pancreatic function and diabetes

Islet replacement is a promising cure for insulin-dependent diabetes but is limited by a massive early cell death following transplantation. Overburden oxidative stress is one of the major factors causing cell damage. We have shown previously that anthocyanins in Chinese bayberry extract protected β cells (INS-1) from hydrogen peroxide (H2O2)-induced apoptosis and decreased grafts' apoptosis after transplantation partially through heme oxygenase-1 (HO-1) up-regulation. In the present study, we observed that H2O2 stimulation induced autophagy in β cells. Inhibition of autophagy increased cell viability and decreased cell death. Anthocyanin pretreatment attenuated oxidative stress-mediated autophagic cell death. Anthocyanins activated antioxidant transcription factor Nrf2 in INS-1 cells, and Nrf2/HO-1 negatively regulated autophagy process. Furthermore, we here demonstrate that autophagy also took place in β cell grafts during the early post-transplantation phase. β Cells pretreated with anthocyanins displayed decreased extent of autophagy after transplantation. Taken together, these findings further supported the conclusion that anthocyanins could serve as a protective agent of β cells and suggested that autophagy might play a role in β cells during transplantation.