4.7 Article

Sesamin alleviates diabetes-associated behavioral deficits in rats: The role of inflammatory and neurotrophic factors

Journal

INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 92, Issue -, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.intimp.2020.107356

Keywords

Diabetes; Sesamin; Behavioral deficits; Neuroinflammation; Neurotrophic factors; Rat

Funding

  1. Ahvaz Physiology Research Center - Ahvaz Jundishapur University of Medical Sciences (Iran) [APRC-9609]

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The study found that sesamin could significantly improve diabetes-associated behavioral deficits, including reducing anxiety/depression-like behaviors, decreasing locomotor/exploratory activities, and improving passive avoidance learning and memory. These improvements may be attributed, at least partly, to the reduction of blood glucose level, inhibition of neuroinflammation, and potentiation of neurotrophic factors.
Neuroinflammation and loss of neurotrophic support have key roles in the pathophysiology of diabetesassociated behavioral deficits (DABD). Sesamin (Ses), a major lignan of sesame seed and its oil, shows antihyperglycemic, anti-oxidative, and neuroprotective effects. The present study was designed to assess the potential protective effects of Ses against DABD and investigate the roles of inflammatory markers and neurotrophic factors in streptozotocin (STZ)-induced diabetic rats. After confirmation of diabetes, Ses (30 mg/kg/day; P.O.) or insulin (6 IU/rat/day; S.C.) was administered to rats for eight consecutive weeks. During the eighth-week period of the study, behavioral functions of the animals were evaluated by employing standard behavioral paradigms. Moreover, inflammation status, neurotrophic factors, and histological changes were assessed in the cerebral cortex and hippocampal regions of the rats. The results of behavioral tests showed that STZ-induced diabetes increased anxiety-/depression-like behaviors, decreased locomotor/exploratory activities, and impaired passive avoidance learning and memory. These DABD were accompanied by neuroinflammation, lack of neurotrophic support, and neuronal loss in both cerebral cortex and hippocampus of the rats. Intriguingly, chronic treatment with Ses improved all the above-mentioned diabetes-related behavioral, biochemical, and histological deficits, and in some cases, it was even more effective than insulin therapy. In conclusion, the results suggest that Ses was capable of improving DABD, which might be ascribed, at least partly, to the reduction of blood glucose level, inhibition of neuroinflammation, and potentiation of neurotrophic factors.

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