The accumulation of advanced glycation end products (AGEs) leads to inflammatory responses via the receptor of AGEs (RAGE) and to neurodegenerative diseases such as Alzheimer’s disease (AD). As part of our continued research interest in identifying dietary agents for AD prevention, herein, we evaluated the neuroprotective effects of anthocyanin-enriched extracts (ACR) purified from six common edible berries, namely, blackberry (Rubus spp.), black raspberry (Rubus occidentalis), blueberry (Vaccinium angustifolium), cranberry (Vaccinium macrocarpon), red raspberry (Rubus idaeus), and strawberry (Fragaria ananassa). ACRs (at 100 µg/mL) were evaluated for their inhibitory effects on the formation of advanced glycation endproducts (AGEs) induced by fructose or reactive carbonyl species, namely, methylglyoxal (MGO). Berry ACRs inhibited fructose- and MGO-induced AGEs formation by 42.4-83.6%, and 26.7-66.3%, respectively. In addition, the MGO trapping capacities of ACRs were evaluated. Berry ACRs scavenged MGO by 13.7–32.8%. Next, the inhibitory effects of berry ACRs on thermo- and MGO-induced fibrillation of beta amyloid (Aβ) were evaluated using the ThT assay. Berry ACRs (at 100 µg/mL) inhibited thermo- and MGO-induced Aβ fibrillation by 24.3-52.1% and 18.4-24.2%, respectively. The neuroprotective effects of berry ACRs were next evaluated in murine microglial (BV-2) cells after exposure to lipopolysaccharide (LPS). Berry ACRs (at 10 µg/mL) reduced nitric oxide levels in media by 19.5-31.6% as compared to BV-2 cells exposed to LPS alone. The neuroprotective effects of the berry ACRs against oxidative and carbonyl induced stresses in human neuronal (SY-SH5Y) cells are being currently evaluated.

Neuroprotective effects of anthocyanin-enriched extracts of common edible berries are mediated by their antioxidant and carbonyl trapping capacities

254th National Meeting (2017)

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