Sesamin reduces diabetes-associated behavioral deficits partly by inhibiting inflammation and potentiation of neurotrophic factors in diabetic rat brain

سال انتشار: 1398
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 514

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شناسه ملی سند علمی:

NSCMED08_192

تاریخ نمایه سازی: 15 دی 1398

چکیده مقاله:

Background and Aim : Neuroinflammation and loss of neurotrophic support play significant roles in the pathophysiology of diabetes-associated behavioral deficits (DABD). Sesamin, a major lignan of sesame seed and its oil, exhibits anti-hyperglycemic, anti-oxidative, anti-inflammatory, and neuroprotective effects. The present study was designed to assess the hypothesis that sesamin partly by inhibiting neuroinflammation and potentiation of neurotrophic factors could attenuate DABD in streptozotocin (STZ)-induced diabetic rat model.Methods : Sesamin (30 mg/kg/day; P.O.) or insulin (6 IU/rat/day; S.C.) were administered to rats immediately after confirmation of diabetes and were continued 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 hippocampus of the rats.Results : The results of behavioral tests showed that STZ-induced diabetes increased anxiety- and depression-like behaviors, decreased exploratory/locomotor activities, and impaired passive avoidance learning. These DABD were associated with neuroinflammation, lack of neurotrophic support, and neuronal loss in both cerebral cortex and hippocampus of the rats. Surprisingly, chronic treatment with sesamin improved all the above-mentioned diabetes-related neurobehavioral deficits at a comparable level with insulin therapy.Conclusion : In conclusion, the results suggest that sesamin was capable of improving DABD, which might be ascribed, at least partly, to the inhibition of neuroinflammation, reduction of blood glucose level, and potentiation of neurotrophic factors.

نویسندگان

Shahab Ghaderi

Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran

Masome Rahsno

Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran

Yaghoob Farbood

Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran

Seyed Esmaeil Khoshnam

Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran

Alireza Sarkaki

Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran

Layasadat Khorsandi

Cellular and Molecular Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran