AMELIORATE EFFECT OF ZINGERONE ON ALUMINUM CHLORIDE AND D-GALACTOSE INDUCED NEUROINFLAMMATION IN THE HIPPOCAMPUS INVOLVES MODULATION OF ERK EXPRESSION
Abstract
This study investigates the ameliorative effect of Zingerone on AICI3/D-galactoseinduced
neuroinflammation in the hippocampus, with a focus on the modulation of
ERK expression, nitric oxide (NO) levels, and myeloperoxidase (MPO) activity.
Twenty eight (28) Adult male albino Wistar rats were divided into fpur groups:
control, AICI3/D-gal only, AICI3/D-gal + Zingerone, and AICI3/D-gal + Donepezil.
The rats were administered with AIC13/D-gal. Intraperitonealy and treated orally with
zingerone and Donepezil for 14days, after which hippocampal tissue samples were
collected and analyzed for ERK expression using immunohistochemistry. NO levels
were measured using a biochemical assay, and MPO activity was assessed to evaluate
oxidative stress and inflammatory responses. AICI3/D-gal administration significantly
increased ERK expression (P < 0.05) in the hippocampus compared to the control
group. Chronic ERK activation has been linked to the progression of
neurodegenerative diseases. Zingerone co-administration significantly reduced ERK
expression (P < 0.05) compared to the AICI3/D-gal group, demonstrating its antiinflammatory
effects. Donepezil administration further reduced ERK'expression to
near-normal levels. Similarly, AICI3/D-gal treatment significantly elevated NO and
MPO levels, indicating increased oxidative stress. Zingerone significantly decreased
NO and MPO levels (P < 0.05) compared to the AICI3/D-gal group, though levels
remained slightly higher than the control. Donepezil reduced both NO and MPO
levels to values closer to the control group. These findings suggest that Zingerone has
therapeutic potential in mitigating neuroinflammation and oxidative stress, making it
a promising candidate for further research in neurodegenerative disease models.
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