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AB239. Icariside II enhances endothelial nitric oxide synthase expression by suppressing miR-155 in diabetic-like human cavernous endothelial cells

BACKGROUND: To investigate the role of Icariside II (ICA II) on endothelial nitric oxide synthase (eNOS) expression regulated by miR-155, the human cavernous endothelial cells (HCECs) were exposed to a diabetic-like environment and treated with ICA II. METHODS: HCECs were treated with 200 µg/mL BSA...

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Detalles Bibliográficos
Autores principales: Guan, Ruili, Lei, Hongen, Yang, Bicheng, Wang, Lin, Li, Huixi, Xin, Zhongcheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4842673/
http://dx.doi.org/10.21037/tau.2016.s239
Descripción
Sumario:BACKGROUND: To investigate the role of Icariside II (ICA II) on endothelial nitric oxide synthase (eNOS) expression regulated by miR-155, the human cavernous endothelial cells (HCECs) were exposed to a diabetic-like environment and treated with ICA II. METHODS: HCECs were treated with 200 µg/mL BSA as the Normal Control group (NC), with 200 µg/mL AGE-BSA plus 250 mg/dL glucose as the diabetes mellitus (DM) group, or with an addition of ICA II in DM group as the treatment group (DM+ICA II). Bioinformatics were first used to predict miRNAs targeting eNOS gene and then potential candidates including miR-155, miR-543, miR-31, miR-429, miR-200b were further verified by real-time PCR in a diabetic-like condition. Expressions levels of miRNAs, eNOS and the receptor for advanced glycation end products (RAGE) were performed by Real-time PCR; Protein expression levels of eNOS and RAGE were analyzed by western blot; nitric oxide (NO) content was detected by DAF-FM DA probe and NaNO(2) standard curve methods. RESULTS: The expression of miR-155 in DM group is significantly higher than that that in the normal control (NC) group, whereas this phenomenon was effectively reversed by ICA II treatment. Furthermore, the miR-155 targeting gene eNOS and its consequent NO product were significantly reduced in DM group, while these changes were also recovered after ICA II treatment. CONCLUSIONS: In this study, we demonstrated that ICA II could promotes eNOS mRNA and protein levels by suppressing miR-155 in HCECs exposed to a diabetic-like environment.