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Protective effects of chronic humanin treatment in mice with diabetic encephalopathy: A focus on oxidative stress, inflammation, and apoptosis.
Bulut, Ferah; Adam, Muhammed; Özgen, Aslisah; Hekim, Munevver Gizem; Ozcan, Sibel; Canpolat, Sinan; Ozcan, Mete.
Afiliación
  • Bulut F; University of Firat, Department of Biophysics, Elazig, Turkey. Electronic address: ferahbulut94@gmail.com.
  • Adam M; University of Firat, Department of Biophysics, Elazig, Turkey. Electronic address: mehmed-adam@hotmail.com.
  • Özgen A; University of Firat, Department of Physiology, Elazig, Turkey. Electronic address: aslisahozgen@gmail.com.
  • Hekim MG; University of Firat, Department of Physiology, Elazig, Turkey. Electronic address: gizemersoz94@gmail.com.
  • Ozcan S; University of Firat, Department of Anaesthesiology and Reanimation, Elazig, Turkey. Electronic address: dr.sibelcozcan@gmail.com.
  • Canpolat S; University of Firat, Department of Physiology, Elazig, Turkey. Electronic address: sinancanpolat@firat.edu.tr.
  • Ozcan M; University of Firat, Department of Physiology, Elazig, Turkey. Electronic address: meteozcan@hotmail.com.
Behav Brain Res ; 452: 114584, 2023 08 24.
Article en En | MEDLINE | ID: mdl-37467966
Diabetes is known to cause cognitive impairments through various mechanisms, including oxidative stress, inflammation, and apoptosis. Humanin (HN) has been shown to have protective effects on cognitive impairments induced by factors such as Aß, muscarinic receptor antagonists, and aging in rodents. However, the mechanisms underlying the protective effects of HN in the prefrontal cortex and hippocampus in the context of diabetes are not well understood. In this study, we aimed to investigate the potential protective role of HN on oxidative stress, inflammation, and apoptosis in mice with diabetes. We divided the mice into four groups, including a control group (treated with saline), a humanin group (treated with 4 mg/kg of HN), a streptozotocin (STZ) group (diabetic control), and an STZ+Humanin group. The mice were administered HN daily for 15 days. Our results showed that in the prefrontal cortex and hippocampus of the diabetes group, oxidative stress parameters, pro-inflammatory cytokines, apoptosis and, blood glucose levels were increased, while antioxidant and anti-inflammatory cytokines were diminished compared to the control group. However, HN treatment was able to modulate these markers, including blood glucose and the markers of oxidative stress, inflammation, and apoptosis. In conclusion, our findings suggest that hyperglycemia, oxidative stress, inflammation, and apoptosis may contribute to the development of diabetes-induced cognitive impairments. By regulating these changes with HN treatment, we may be able to positively contribute to the treatment of cognitive impairments induced by diabetes.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Glucemia / Diabetes Mellitus Límite: Animals Idioma: En Revista: Behav Brain Res Año: 2023 Tipo del documento: Article Pais de publicación: Países Bajos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Glucemia / Diabetes Mellitus Límite: Animals Idioma: En Revista: Behav Brain Res Año: 2023 Tipo del documento: Article Pais de publicación: Países Bajos