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Protective effects of salvianolic acid B against hydrogen peroxide-induced apoptosis of human umbilical vein endothelial cells and underlying mechanisms

Salvianolic acid B (Sal B) is a water-soluble active component of Danshen and has anti-atherosclerotic effects. The present study aimed to evaluate the cytoprotective effects of Sal B against hydrogen peroxide (H(2)O(2))-induced oxidative stress damage in human umbilical vein endothelial cells (HUVE...

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Detalles Bibliográficos
Autores principales: Gao, Shan, Li, Shiqin, Li, Qin, Zhang, Fuyong, Sun, Mengqi, Wan, Zilin, Wang, Shurong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6605496/
https://www.ncbi.nlm.nih.gov/pubmed/31173197
http://dx.doi.org/10.3892/ijmm.2019.4227
Descripción
Sumario:Salvianolic acid B (Sal B) is a water-soluble active component of Danshen and has anti-atherosclerotic effects. The present study aimed to evaluate the cytoprotective effects of Sal B against hydrogen peroxide (H(2)O(2))-induced oxidative stress damage in human umbilical vein endothelial cells (HUVECs) and investigate the underlying mechanisms. It was revealed that Sal B protected the cells from H(2)O(2)-induced damage, as indicated by MTT results showing enhanced cell viability and by flow cytometric analysis showing reduced apoptosis of cells challenged with H(2)O(2). Furthermore, as an underlying mechanism, the enhancement of autophagy was indicated to be accountable for the decrease in apoptosis, as Sal B caused the upregulation of light chain 3-II and Beclin-1, and downregulation of p62 under H(2)O(2)-induced oxidative stress. Finally, Sal B increased the phosphorylation of AMP kinase (AMPK) and decreased the phosphorylation of mammalian target of rapamycin (mTOR), but had no effect on the phosphorylation of AKT. In conclusion, the present study revealed that Sal B protects HUVECs from oxidative stress, at least partially by promoting autophagy via activation of the AMPK pathway and downregulation of the mTOR pathway.