Abstract

Anxiety, hippocampus synaptic plasticity deficit, as well as pro-inflammatory cytokines, are involved in Alzheimer's disease (AD). The present study is designed to evaluate the possible therapeutic effect of crocin on anxiety-like behaviours, hippocampal synaptic plasticity and neuronal shape, as well as pro-inflammatory cytokines in the hippocampus using in vivo amyloid-beta (A beta) models of AD. The A beta peptide (1-42) was bilaterally injected into the frontal-cortex. Five hours after the surgery, the rats were given intraperitoneal (IP) crocin (30 mg/kg) daily up to 12 days. Elevated plus maze results showed that crocin treatment after bilateral A beta injection significantly increased the percentage of spent time into open arms, frequency of entries, and percentage of entries into open arms as compared with the A beta group. In the open field test, the A beta+crocin group showed a higher percentage of spent time in the centre and frequency of entries into central zone as compare with the A beta treated animals. Administering crocin increased the number of soma, dendrites and axonal arbores in the CA1 neurons among the rats with A beta neurotoxicity. Cresyl violet (CV) staining showed that crocin increased the number of CV-positive cells in the CA1 region of the hippocampus compared with the A beta group. Silver-nitrate staining indicated that crocin reduced neurofibrillary tangle formation induced by A beta. Crocin treatment attenuated the expression of TNF-alpha and IL-1 beta mRNA in the hippocampus compared with the A beta group. Our results suggest that crocin attenuated A beta-induced anxiety-like behaviours and neuronal damage, and synaptic plasticity loss in hippocampal CA1 neurons may via its anti-inflammatory effects.