Acrylamide (AA) is a widespread environmental and dietary-derived neurotoxin, which can induce oxidative stress and associated inflammation in the brain. Anthocyanins widely occur as natural antioxidant and anti-inflammatory phytochemicals. Herein, the protective effects of blueberry anthocyanins extract (BAE) against AA-induced neurotoxicity were investigated in rats. The rats were pretreated with BAE (175 mg/kg body weight/day) by oral gavage for the first 7 days, followed by the co-administration of BAE and AA (35 mg/kg body weight/day) by oral gavage for the next 12 days. Results showed that BAE significantly decreased the malondialdehyde (MDA) production, and increased glutathione (GSH) and antioxidant enzyme levels; and it also suppressed microglial activation, astrocytic reaction, and pro-inflammatory cytokine expressions. Furthermore, BAE elevated the extracellular signal-related kinase (ERK)/cAMP response elements binding protein (CREB)/brain-derived neurotrophic factor (BDNF) pathway, and relieved the accumulation of amyloid beta (Aβ) 1-42 and 1-40 after AA exposure. Consequently, AA-induced neuronal necrosis and downregulation of synaptosomal-associated protein 25 (SNAP-25) were attenuated by BAE in the hippocampus and cerebral cortex. In conclusion, BAE can exert a protective function on neurons and synapses against AA-induced oxidative stress and neuroinflammation.
Copyright © 2022 Zizhuang Fang et al.