Neuroprotective Effect of Barbaloin on Streptozotocin-Induced Cognitive Dysfunction in Rats via Inhibiting Cholinergic and Neuroinflammatory Cytokines Pathway?TNF-α/IL-1β/IL-6/NF-ΚB

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-kappa B), IL-1 beta (interleukin-1 beta), IL-6, and tumor necrosis factor-alpha (TNF-alpha) 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-kappa B, IL-6, TNF-alpha, and IL1 beta levels were also altered. In conclusion, the findings revealed that barbaloin had a protective impact against cognitive dysfunction caused by STZ.

Automated summary

Streptozotocin (STZ) impairs memory in rats through various mechanisms including cholinergic dysfunction, oxidative stress, hyperglycemia, and alterations in glucagon-like peptide (GLP). Barbaloin has been shown to have pharmacological effects but its effectiveness in improving STZ-induced memory dysfunction is not clear. In this study, barbaloin treatment significantly improved memory and cognitive functions, as measured by Y-maze and Morris water maze tests. The levels of oxidative stress markers, cholinergic dysfunction indicators, and inflammatory cytokines were also regulated by barbaloin treatment. These findings suggest that barbaloin has a protective impact against cognitive dysfunction caused by STZ.