Embelin Abrogates Amyloid-β-Induced Neurotoxicity and Prevents Cognitive
decline in Rats: Possible Role of Hippocampal Neurochemistry
Abstract
Backgound: Extracellular deposits of amyloid-β (Aβ) in neuronal synapse
have been considered as a major hallmark of Alzheimer’s disease.
Purpose: Here in we have investigated the neuroprotective potential of
embelin Aβ-42 induced neurotoxicity in rats. Material and Methods:
Amyloid β1-42 oligomer was infused (3nmol/3µl) intracerebroventrically
twice on day-1to induced Alzheimer’s type dementia in rats. Spatial and
non- spatial memory was assessed at different time intervals and
terminally biochemical, neurochemical and neuroinflammatory parameters
were determined in rat hippocampal brain tissue. One week following
Aβ1-42 infused rats were treated with different doses of embelin (2.5, 5
and 10mg/kg/p.o.) till 21st day. Results: Amyloid β1-42 infusion
produced significant deterioration in learning and memory while
hippocampal tissue showed elevation in AChE activity, oxidative stress,
and pro-inflammatory cytokine levels (TNF-α, IL-β etc.) and disturbed
pattern of GABA/glutamate levels in Aβ1-42 infused rats. On the other
side, embelin significantly attenuated Aβ1-42 induced cognitive deficit
& other biochemical changes in rats. Embelin treated rats showed
improved learning and memory was able to reduce the burden of
hippocampal oxidative stress and pro-inflammatory cytokines and also
restored the GABA/glutamate balance in rats. Conclusion and Implication:
The pro-cognitive effect of embelin may be due to its antioxidant and
anti-inflammatory actions. The observed results indicate the therapeutic
potential of embelin in cognitive disorders. Key words: Alzheimer’s
disease; Embelin; Amyloid-β; Neuroprotection; Dementia; Cognitive
deficit.