Effect of icariin in a rat model of colchicine-induced cognitive deficit: role of β-amyloid proteolytic enzymes
Abstract: The deposition of β-amyloid plaques, either due to their over-production or insufficient clearance, is an important pathological process in cognitive impairment and dementia. Icariin (ICA), a flavonoid compound extracted from Epimedium, has recently gained attention for numerous age-related diseases, such as neurodegenerative diseases. We aimed to explore the possible neuro-protective effect of ICA supplementation in colchicine-induced cognitive deficit rat model and exploring its effect on the β-amyloid proteolytic enzymes. The study included four groups (10 rats each): normal control, untreated colchicine, colchicine + 10 mg/kg ICA, and colchicine + 30 mg/ kg ICA. Results revealed that intra-cerebro-ventricular colchicine injection produced neuronal morphological damage, β amyloid deposition, and evident cognitive impairment in the behavioral assessment. Icariin supplementation in the two doses for 21 days attenuated neuronal death, reduced the β amyloid levels, and improved memory consolidation. This was associated with modulation of the proteolytic enzymes (Neprilysin, Matrix Metalloproteinase-2, and insulin-degrading enzyme) concluding that β-amyloid enzymatic degradation may be the possible therapeutic target for ICA.
Keywords: Icariin / neprilysin / insulin-degrading enzyme / matrix metalloprotinase-2 / AD: Alzheimer’s disease / ACSF: artificial cerebrospinal fluid / ECM: extracellular matrix / ICA: Icariin / IDE: insulin-degrading enzyme / ICV: intra-cerebro-ventricular / MMP: matrix metalloproteinase / NEP: neprilysin / Aβ: β amyloid / NF-κB: Nuclear factor-kappa B
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