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AB199. Resveratrol, an activator of SIRT1, restores erectile function in streptozotocin-induced diabetic rats

OBJECTIVE: The high incidence of erectile dysfunction (ED) in diabetes highlights the need for good treatment strategies. Recent evidence indicates that silent information regulator 2 related enzymes 1 (Sirtuin1, SIRT1) plays a critical role in endothelial homeostasis, apoptosis and oxidative stress...

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Detalles Bibliográficos
Autores principales: Yu, Wen, Dai, Yutian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4708748/
http://dx.doi.org/10.3978/j.issn.2223-4683.2015.s199
Descripción
Sumario:OBJECTIVE: The high incidence of erectile dysfunction (ED) in diabetes highlights the need for good treatment strategies. Recent evidence indicates that silent information regulator 2 related enzymes 1 (Sirtuin1, SIRT1) plays a critical role in endothelial homeostasis, apoptosis and oxidative stress. To explore the role of SIRT1 in the pathogenesis of diabetic ED and the role of resveratrol in the treatment of diabetic ED, resveratrol (a activator of SIRT1) was administered to rats with streptozocin (65 mg/kg)-induced diabetes. METHODS: Erectile function, cavernous structure, tissue protein expression of SIRT1, p53, FOXO3a and superoxide dismutase (SOD) activity and malondialdehyde (MDA) in the corpora cavernosa were studied. RESULTS: SIRT1 was expressed in cavernosal tissue and it was down-regulated in the corpora of diabetic rats. Administration of resveratrol up-regulated the expression of SIRT1, partially restored erectile function. In contrast, it down-regulated the expression of p53 and FOXO3a. Furthermore, resveratrol-treated group revealed an improved content of smooth muscle, SOD activity and MDA as compared with the diabetic group. CONCLUSIONS: Therefore, the cavernous SIRT1 plays a role in modulating erectile function in corpora cavernosa and is involved in the pathogenesis of diabetic ED. Overexpression of SIRT1 can restore diabetic ED through suppressing apoptosis and resisting oxidative stress.