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J Agric Food Chem. 2013 Sep 18;61(37):8765-72. doi: 10.1021/jf4012399. Epub 2013 Sep 6.

Anthocyanins from Chinese bayberry extract activate transcription factor Nrf2 in β cells and negatively regulate oxidative stress-induced autophagy.

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Department of Surgery (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), Second Affiliated Hospital, School of Medicine, Zhejiang University , No. 88 Jiefang Road, Hangzhou, Zhejiang Province 310009, People's Republic of China.


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.

[Indexed for MEDLINE]

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