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Atorvastatin protects cardiomyocytes against OGD/R-induced apoptosis by inhibiting miR-199a-5p

The present study aimed to evaluate the protective effects of atorvastatin against myocardial ischemia/reperfusion (I/R) injury in cardiomyocytes and its underlying mechanisms. The direct cytotoxic effects of oxygen-glucose deprivation/reperfusion (OGD/R) on cardiomyocytes with and without atorvasta...

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Detalles Bibliográficos
Autores principales: Li, Yong, Jiang, Ting, Fu, Xingli, Xu, Hao, Ji, Jianguo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5646958/
https://www.ncbi.nlm.nih.gov/pubmed/28765953
http://dx.doi.org/10.3892/mmr.2017.7084
Descripción
Sumario:The present study aimed to evaluate the protective effects of atorvastatin against myocardial ischemia/reperfusion (I/R) injury in cardiomyocytes and its underlying mechanisms. The direct cytotoxic effects of oxygen-glucose deprivation/reperfusion (OGD/R) on cardiomyocytes with and without atorvastatin pretreatment were evaluated. The effects of atorvastatin on the expression of glycogen synthase kinase-3β (GSK-3β) and microRNA (miR)-199a-5p were determined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analyses. In addition, the expression levels of GSK-3β in cells with miR-199a-5p upregulation and downregulation were detected using RT-qPCR, western blot and immunohistochemical analyses. Pretreatment with atorvastatin significantly improved the recovery of cell viability from OGD/R (P<0.05). In addition, atorvastatin pretreatment significantly increased the expression of GSK-3β at the mRNA and protein levels, and the expression of miR-199a-5p at the mRNA level (all P<0.05). The upregulation and downregulation of miR-199a-5p respectively decreased and increased the expression of GSK-3β at the mRNA and protein levels. These results suggested that atorvastatin provided cardioprotective effects against I/R injury via increasing the expression of GSK-3β through the inhibition of miR-199a-5p.