Chronic ethanol exposure is known to cause neuronal damage in both humans and experimental animal models.
Ethanol treatment induces neurotoxicity via the generation of reactive oxygen species (ROS), while anthocyanins
(extracted from black soybean) and ascorbic acid (vitamin C) are free radical scavengers that can be used as
neuroprotective agents against ROS. In this study the underlying neuroprotective potential of black soybean anthocyanins
and vitamin C was determined. For this purpose, adult rats were exposed to 10% (v/v) ethanol for 8 weeks, followed by
co-treatment with anthocyanins (24 mg/kg) and vitamin C (100 mg/kg) during the last 4 weeks. Our results showed that
ethanol administration increased the expression of γ -aminobutyric acid B1 receptor (GABAB1R) and induced neuronal
apoptosis via alterations to the Bax/Bcl-2 ratio, release of cytochrome C and activation of caspase-3 and caspase-9.
Anthocyanins alone and supplementation with vitamin C showed an additive effect in reversing the trend of apoptotic
signals induced by ethanol in the cortex and hippocampus. Consequently, anthocyanins also decreased the expression of
poly (ADP ribose) polymerase-1 induced by ethanol and prevented DNA damage. Furthermore, anthocyanins and vitamin
C reversed the ethanol-induced expression of GABAB1R and its downstream signaling molecule phospho-cAMP response
element binding protein. Moreover, histopathology and immunohistochemistry results showed that anthocyanins and
vitamin C significantly reduced ethanol-induced neuronal cell death. Our study revealed a neuroprotective role of
anthocyanins and vitamin C via modulation of GABAB1R expression in the adult brain. Hence, we suggest that
anthocyanins or co-treatment with anthocyanins and vitamin C may be a new and potentially effective neuroprotective
agent for alcohol abuse.
Keywords: Anthocyanins, Apoptotic signaling pathway, γ-aminobutyric acid B1 receptor, Neuroprotection, protein kinase AcAMP
response element binding protein pathway.
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