keywords: Diabetes, Cellgevity®, acetylcholine esterase, cholinergic dysfunction, oxidative stress
Reactive-radicals’ mediated neurochemical changes caused by diabetic hyperglycemia, participate in cognitive impairment and neurodegeneration. The present study investigated the effect of Cellgevity® (marketed glutathione enhancer) on cognitive function, inflammation, and oxidative stress in STZ-diabeticrats. Behavioural and cognitive parameters were assessed and the cerebral cortex region was assessed for acetylcholine esterase activity, oxidative stress markers, and inflammation. STZ-diabetes impaired rats’ memory and it induced anxiety-like behaviour. It led to at least 2 fold increases in acetylcholinesterase activity, levels of TNF-α, nitrite, and lipid peroxidation respectively in the cerebral cortex. It also caused 3.25 fold and 1.62 fold decreases in the activities of glutathione peroxidase and superoxide dismutase respectively compared to non-diabetic control. Separate treatment of diabetic rats with Cellgevity® (25 or 40 mg/kgbw)for 28 days significantly attenuated cognitive deficit, increased acetylcholinesterase activity, decreased oxidative/nitrosative stress and inflammation. Our results show the involvement of oxidative/nitrosative and inflammatory events in diabetes-induced neurodegeneration in rats and it presents the possible therapeutic potentials of Cellgevity® in ameliorating these diabetic-associated neurochemical dysfunctions. Cellgevity® prevents the increase in acetylcholinesterase activity, showing that it can modulate cholinergic neurotransmission and consequently improve cognition. Taken together, our results confirm the capacity of Cellgevity® as an antioxidant, to neutralizeexcess free radicals generated by diabetes disease and consequently stalldiabetes-neurodegeneration.