Frontiers in behavioral neuroscience
Therapeutic potential of Cola nitida against dexamethasone- and scopolamine-induced cognitive and cardiac dysfunction
By Adedayo LD, Michael OS, Ayilara GO and 7 others.
Abstract
Background
Cognitive dysfunction and cardiometabolic disturbances frequently coexist in neurological and metabolic disorders. Chronic systemic inflammation in cardiometabolic syndrome may promote neuroinflammation, damaging neurons and synapses and impairing memory pathways. Cola nitida is a medicinal plant widely recognized for its stimulant and therapeutic properties, yet its neuroprotective and cardiometabolic effects remain underexplored.
Objective
This study investigated the effects of methanol extract of Cola nitida (CN) in a mouse model of memory and metabolic dysfunction induced by scopolamine and dexamethasone.
Methods
Male mice were randomly divided into six groups (n = 5): control (saline), scopolamine (3 mg/kg), scopolamine + dexamethasone (0.2 mg/kg), CN (50 mg/kg) + scopolamine, CN + scopolamine + dexamethasone, and donepezil (1 mg/kg) + scopolamine + dexamethasone. Treatments lasted 7 days, followed by behavioral testing (Morris Water Maze, Y-Maze). Biochemical analyses included acetylcholinesterase activity, oral glucose tolerance, lactate/LDH, oxidative stress markers, and lipid profiles. Hippocampal histology assessed neurodegeneration, while molecular docking evaluated CN phytochemicals against proteins linked to glucose metabolism, oxidative stress, and cholinergic signaling.