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Dietary Supplements Protect Retinal Pigment Epithelial Cells From Hyperglycemic Damage
Author(s) -
Lin Dingbo,
Zhang Yug,
Medeiros Denis M
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.230.6
Subject(s) - ampk , microbiology and biotechnology , phosphorylation , apoptosis , chemistry , protein kinase a , amp activated protein kinase , blot , biochemistry , kinase , biology , gene
Objective To determine the protective effects of wolfberry on hyperglycemic damage in retinal pigment epithelial cells. Methods Human retinal pigment epithelial ARPE‐19 cells were treated with 36 mM glucose for 60 hrs, with or without 1 mg/mL crude wolfberry extracts. PKCgamma activation was determined by enzyme activity assay. Gap junction activity was determined by scrape loading/dye transfer assay. Western blotting was used to determined activation of AMP‐activated protein kinase (AMPK), acetyl‐CoA carboxylase (ACC), and apoptosis‐inducing factor (AIF). Results High glucose‐activated PKCgamma phosphorylated Connexin 50 (Cx50) and Cx57 on serines, and subsequently inhibited gap junction activity. Wolfberry extracts abolished the effects of high glucose on PKCgamma activation. Application of wolfberry extracts abolished the inhibitory effect of high glucose on AMPK activation, completely restored ACC phosphorylation by AMPK, and inhibited AIF translocation out of mitochondria. Conclusions High glucose‐induced AIF‐dependent apoptosis would be protected by application of wolfberry extracts through restoration of cellular gap junctional communication and rebalance of cellular energy homeostasis.