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Antioxidant effect of angiotensin (1-7) in the protection of pancreatic β cell function

It is well known that the local renin-angiotensin system (RAS) is activated in the diabetic state, which results in an increase in the level of oxidative stress injury to pancreatic β cells. The angiotensin-converting enzyme 2 (ACE2)/angiotensin (1-7) [Ang (1-7)]/Mas axis is a negative regulator of...

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Detalles Bibliográficos
Autores principales: Zhang, Fen, Liu, Chang, Wang, Lei, Cao, Xi, Wang, Ying Ying, Yang, Jin Kui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4991744/
https://www.ncbi.nlm.nih.gov/pubmed/27430410
http://dx.doi.org/10.3892/mmr.2016.5514
Descripción
Sumario:It is well known that the local renin-angiotensin system (RAS) is activated in the diabetic state, which results in an increase in the level of oxidative stress injury to pancreatic β cells. The angiotensin-converting enzyme 2 (ACE2)/angiotensin (1-7) [Ang (1-7)]/Mas axis is a negative regulator of the classical renin-angiotensin system. In order to investigate the antioxidant effect of Ang (1-7) on pancreatic β cells, INS-1 cells were cultured and oxidative stress was induced by treatment with H(2)O(2). Glucose-stimulated insulin secretion (GSIS), the generation of reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and glucose-stimulated calcium (GSCa) responses in β cells were determined following treatment with Ang (1-7). It was observed that H(2)O(2) significantly impaired the insulin secreting function, increased the production of ROS, and also decreased the levels of GSCa and MMP. Pre-treatment with Ang (1-7) alleviated these effects and treatment with A779 [antagonist of Ang (1-7)] prevented the effects of Ang (1-7). Based on these findings, it was concluded that Ang (1-7) can protect pancreatic β cells from oxidative injury and such protection can be blocked by its antagonist A779.