The recent investigation was to ascertain whether europinidin could
defend rats against scopolamine- tempted deficits in learning and
memory. Wistar rats were arbitrarily separated into four clusters and
treated as follows: Cluster 1 (normal control) and Cluster 2
(scopolamine-SCOP) received oral administration of 3 ml/kg of 0.5%
sodium CMC (vehicle). Clusters 3 and 4 received europinidin (p.o. lower
dose-10 and higher-20 mg/kg, respectively) for a 14-day period. The
ability to move spontaneously, recall information, and learn were
assessed in rats for 15-day, animals were placed for euthanasia, and
analyzed for acetylcholine esterase (AChE), choline acetyltransferase
(ChAT), antioxidant (CAT, SOD, GSH, and MDA), nitrites,
anti-inflammatory (TNF-α, IL-1β, IL-6, and IL-10) and brain-derived
neurotrophic factor (BDNF). SCOP caused the animals to lose their
memory. SCOP altered the activities of AChE and ChAT, decreased GSH,
SOD, and CAT quantity attenuated the levels of IL-10, BDNF, and improved
levels of MDA, nitrate, IL-1β, IL-6, and TNF-α in brain tissue.
Europinidin effectively reduced the neurobehavioral deficits, oxidative
stress, and neuroinflammatory markers affected by SCOP in the treated
rats as well as reverted the AChE, ChAT, and BDNF levels back to normal,
europinidin lessens the reminiscence impairment affected by scopolamine
in rats.