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Curcumin alleviates liver oxidative stress in type 1 diabetic rats

The aim of the present study was to determine the effects of curcumin on antioxidants using a rat model of type 1 diabetes. Seven-week-old male Sprague-Dawley rats were injected with Streptozotocin (STZ) intraperitoneally to induce this model, and then treated with 1.0% curcumin (weight ratio) mixed...

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Detalles Bibliográficos
Autores principales: Xie, Zhenglu, Wu, Binbin, Shen, Guozhi, Li, Xiaqing, Wu, Qianying
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5780069/
https://www.ncbi.nlm.nih.gov/pubmed/29115468
http://dx.doi.org/10.3892/mmr.2017.7911
Descripción
Sumario:The aim of the present study was to determine the effects of curcumin on antioxidants using a rat model of type 1 diabetes. Seven-week-old male Sprague-Dawley rats were injected with Streptozotocin (STZ) intraperitoneally to induce this model, and then treated with 1.0% curcumin (weight ratio) mixed in their diet for 21 days. The present study included three groups: Control group (NC), diabetic rat model group (DC) and a curcumin treated group (Diab-Cur). The results demonstrated that curcumin treatment markedly decreased the blood glucose levels, plasma malondialdehyde concentration and plasma activity of glutathione peroxidase (GSH-Px) and catalase (CAT); however, it increased the plasma superoxide dismutase (SOD) and insulin levels. Curcumin treatment increased the expression of the CAT, GSH-Px, HO-1 and norvegicus NAD(P)H quinone dehydrogenase 1, and decreased the SOD1 expression, which, led to a diminished oxidative stress status. In addition, curcumin treatment significantly increased the protein expression of Keap1 in the Diab-Cur group when compared with the DC group, decreased cytosolic concentrations of Nrf2 while increasing nuclear accumulation of Nrf2. The results provide evidence that oxidative stress in the STZ-induced diabetic rat model may be attenuated by curcumin via the activation of the Keap1-Nrf2-ARE signaling pathway, as evidenced by a decrease in the blood glucose concentration and an increase in the transcription of several antioxidant genes.