Coffee is one of the most frequently consumed beverages in the world and its popularity continues to increase. In fact, our previous study has shown that coffee extract and chlorogenic acid, a major phenolic compound in coffee, protect hypoxia induced retinal degeneration.The aim of this study was to determine whether 3,4-dihydroxyhydrocinnamic acid (DHCA) and dihydroferulic acid (DHFA), the most abundant metabolites detected in human plasma after coffee consumption, have retina protective effects against peroxynitrite (ONOO-) in vitro and N-methyl-d-aspartate (NMDA)-induced retinal degeneration in vivo.Treatment with DHCA and DHFA could reduce intracellular reactive oxygen species stimulated by 3-morpholinosydnonimine (SIN-1), a peroxynitrite donor, in transformed retinal ganglion cell (RGC-5). Protective effects against oxidative stress induced apoptosis was determined by analyzing the nuclear fragmentation by fluorescence microscopy and mitochondrial membrane potential by flow cytometry. Western blot data revealed that coffee metabolites induced an increase in sirtuin (SIRT) 1 expression and mediated overexpression of the levels of endoplasmic reticulum stress marker, CCAAT/enhancer-binding protein homologous protein (CHOP), and phospho-ERK (pERK).We investigated the effect of detected metabolites on the NMDA-induced retinal degeneration in ICR mice. Retinal degeneration caused by NMDA in mice was significantly protected by simultaneous injection of coffee metabolites. The up-regulation of poly ADP-ribose polymerase (PARP) and down-regulation of neurofilament light (NF-L) in NMDA-induced retinal damage were significantly attenuated by coffee metabolite.Our results suggest that selected coffee metabolites provide effective protection against peroxynitrite- and NMDA-induced retinal degeneration.

Coffee metabolites, 3,4-dihydroxyhydrocinnamic acid (DHCA) and dihydroferulic acid (DHFA), protect oxidative stress induced retinal degeneration

248th National Meeting (2014)

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