Streptozotocin (STZ) impairs memory in rats through altering the central nervous systems (CNS) as a result of impaired
cholinergic dysfunction, oxidative stress, persistent
hyperglycemia, and alterations in the
glucagon-like peptide (GLP). In this model
cholinergic agonist,
antioxidant and
antihyperglycemic treatment has been shown to have positive effects.
Barbaloin has a variety of pharmacological effects. However, there is no evidence on how
barbaloin improves memory dysfunction caused by STZ. Thus, we examined its effectiveness against cognitive damage caused by STZ at a dose of 60 mg/kg i.p. in Wistar rats.
Blood glucose levels (BGL) and
body weight (BW) were assessed. To assess learning and memory skills, the Y-maze test and Morris water maze (MWM) test were utilized.
Superoxide dismutase (SOD),
malondialdehyde (MDA),
catalase (CAT), and
glutathione (GSH) as oxidative stress markers were regulated to reverse the cognitive deterioration, and
choline-acetyltransferase (ChAT) and acetyl-
cholinesterase (AChE) as indicators of
cholinergic dysfunction,
nuclear factor kappa-B (NF-κB), IL-1β (interleukin-1β),
IL-6, and
tumor necrosis factor-α (TNF-α) contents were used.
Barbaloin treatment thereby significantly decreased the BW and learning and memory capacities, resulting in substantial behavioral improvement in the Y-maze and MWM test. BGL, SOD, CAT, MDA, GSH, AChE, ChAT, NF-κB,
IL-6, TNF-α, and IL-1β levels were also altered. In conclusion, the findings revealed that
barbaloin had a protective impact against
cognitive dysfunction caused by STZ.