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Sesamin alleviates diabetes-associated behavioral deficits in rats: The role of inflammatory and neurotrophic factors.
Ghaderi, Shahab; Rashno, Masome; Nesari, Ali; Khoshnam, Seyed Esmaeil; Sarkaki, Alireza; Khorsandi, Layasadat; Farbood, Yaghoob; Rashidi, Khodabakhsh.
Afiliação
  • Ghaderi S; Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran; Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
  • Rashno M; Department of Physiology, Faculty of Medicine, Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
  • Nesari A; Department of Pharmacology, School of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
  • Khoshnam SE; Department of Physiology, Faculty of Medicine, Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
  • Sarkaki A; Department of Physiology, Faculty of Medicine, Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
  • Khorsandi L; Cellular and Molecular Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
  • Farbood Y; Department of Physiology, Faculty of Medicine, Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Electronic address: farbood_y@yahoo.com.
  • Rashidi K; Research Center of Oils and Fats, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Int Immunopharmacol ; 92: 107356, 2021 Mar.
Article em En | MEDLINE | ID: mdl-33440305
ABSTRACT
Neuroinflammation and loss of neurotrophic support have key roles in the pathophysiology of diabetes-associated behavioral deficits (DABD). Sesamin (Ses), a major lignan of sesame seed and its oil, shows anti-hyperglycemic, 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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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Ansiedade / Lignanas / Depressão / Diabetes Mellitus Experimental / Dioxóis / Inflamação / Transtornos da Memória / Fatores de Crescimento Neural Tipo de estudo: Etiology_studies / Prognostic_studies / Risk_factors_studies Limite: Animals Idioma: En Ano de publicação: 2021 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Ansiedade / Lignanas / Depressão / Diabetes Mellitus Experimental / Dioxóis / Inflamação / Transtornos da Memória / Fatores de Crescimento Neural Tipo de estudo: Etiology_studies / Prognostic_studies / Risk_factors_studies Limite: Animals Idioma: En Ano de publicação: 2021 Tipo de documento: Article