Caffeine and Camellia sinensis enhance cognition and decrease acetylcholinesterase activity in scopolamine-induced memory loss in female Swiss mice
Keywords:Acetylcholinesterase, Caffeine, Green tea, Memory loss, Scopolamine
Caffeine and Camellia sinensis (green tea) has been known to have positive effect on memory. The present study investigated the possible effect of caffeine and green tea co-administration on oxidative stress markers, inflammatory marker and acetylcholine esterase activity in scopolamine-induced memory loss in female Swiss mice. Memory behavioral tests using Y-maze and Morris water maze was carried out, followed by oxidative stress biomarkers, acetylcholinesterase activity and Tumor Necrosis Factor alpha (TNF-?) evaluation from the mice brain tissues after caffeine and green tea administration. Scopolamine administered intraperitoneally at a dose of 1mg/kg Body Weight (BW) for 7 days significantly reduced the percent alternation of the mice in Y-maze thus, increased acetylcholinesterase activity and increased TNF-? level. However, caffeine administered orally at a dose 50mg/kg BW and green tea administered orally at a dose of 60mg/kg BW increased the percent alternation significantly, reduced acetylcholinesterase activity and reduced the TNF-? level significantly. Oxidative stress markers evaluated GSH and MDA, showed no significant difference across all groups. These findings showed scopolamine has a deteriorating effect on cognition by increasing acetylcholinesterase activities thus mopping out acetylcholine at a faster rate. However, caffeine and green tea singly and in combination restored cognition, reduced acetylcholinesterase activity and restored TNF-? level. The neuroprotective effect of caffeine and green tea was compared to that of Donepezil, an established cognition enhancing drug and the effect was agonistic. The ability of caffeine and green tea to reduce acetylcholinesterase activity could be the mechanism for the ability to enhance memory. The ability of these compounds in restoring TNF-? level also further potentiates their neuroprotective capability.
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