Fucoidan ameliorates scopolamine-induced neuronal impairment and memory dysfunction in rats via activation of cholinergic system and regulation of cAMP-response element-binding protein and brain-derived neurotrophic factor expressions

Abstract

Effect of fucoidan (FCN) treatment on improving memory defects caused by administration of scopolamine (SCO) to the rats was examined. The effects of FCN on the acetylcholinergic system as well as the expression of cAMP-response elementbinding protein (CREB) and brain-derived neurotrophic factor (BDNF) mRNAs in the hippocampus were also investigated. Male rats were administered daily doses for 14 days of FCN (10, 20, and 50 mg/kg, i.p.) 30 min before scopolamine injection (2 mg/kg, i.p.). Daily administration of FCN improved memory impairment as measured by the passive avoidance test (PAT) and reduced the escape latency for finding the platform in the Morris water maze (MWM) test. Administration of FCN significantly alleviated memory-associated decreases in cholinergic immunoreactivity and restored the expression level of BDNF and CREB mRNAs in the hippocampus. Additionally, FCN significantly decreased the expression of pro-inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) mRNAs in the hippocampus. These results demonstrated that FCN has significant neuroprotective effects against neuronal impairment and memory dysfunction caused by scopolamine in rats. Thus, these findings suggest that FCN is useful as a therapeutic agent for improving cognitive functioning via stimulation of cholinergic enzyme activities and regulation of CREB and BDNF expressions in the brain.