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Resveratrol protects vascular smooth muscle cells against high glucose-induced oxidative stress and cell proliferation in vitro

Rong Guo, Weiming Li, Baoxin Liu, Shuang Li, Buchun Zhang, Yawei Xu

Department of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China (mainland)

Med Sci Monit Basic Res 2014; 20:82-92

DOI: 10.12659/MSMBR.890858

Available online: 2014-06-27

Published: 2014-06-27


Background: Resveratrol exhibits beneficial effects against numerous degenerative diseases at different stages of pathogenesis. This study investigated potential mechanisms and resveratrol effects on high glucose (HG)-induced oxidative stress (30 mM d-glucose, 30 min) and cell proliferation (30 mM d-glucose, 24 h) in vascular smooth muscle cells (VSMCs).
Material and Methods: Intracellular reactive oxygen species (ROS) generation was detected by 2’,7’-dichlorofluorescein diacetate (DCFH-DA). Total antioxidant capacity (TAC), malonyldialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD) were measured to evaluate oxidative stress. VSMC proliferation was measured by CCK-8 assays and through propidium iodide-based cell cycle analysis. Expression of NAD(P)H oxidase, proliferation proteins, and cell signalling were assessed by immunoblot analysis.
Results: Co-treatment of primary cultures of VSMCs with 1–100 μM resveratrol decreased HG-induced ROS overproduction (P<0.05). Resveratrol also abolished HG-induced phosphorylation of oxidase subunit p47 phox and reduced HG-induced cyclin D1, cyclin E, and PCNA expression in a concentration-dependent manner. Furthermore, resveratrol (10 μM) attenuated HG-induced phosphorylation of Akt, p38 mitogen-activated protein kinase (MAPK), ERK 1/2, and JNK1/2 without affecting total levels. HG stimulation enhanced downstream IκB-α phosphorylation and NF-κB activity, and resveratrol repressed these effects.
Conclusions: Resveratrol inhibits HG-induced oxidative stress and VSMC proliferation by suppressing ROS generation, NADPH oxidase, Akt phosphorylation, p38 MAPK/JNK/ERK phosphorylation, and IκB-α and NF-κB activities.

Keywords: Biological Markers - metabolism, Animals, Cell Cycle - drug effects, Cell Proliferation - drug effects, Cell Survival - drug effects, Cells, Cultured, Cytoprotection - drug effects, Extracellular Signal-Regulated MAP Kinases - metabolism, Glucose - toxicity, I-kappa B Proteins - metabolism, JNK Mitogen-Activated Protein Kinases - metabolism, Models, Biological, Muscle, Smooth, Vascular - pathology, Myocytes, Smooth Muscle - pathology, NADPH Oxidase - metabolism, Oxidation-Reduction - drug effects, Oxidative Stress - drug effects, Phosphorylation - drug effects, Protective Agents - pharmacology, Proto-Oncogene Proteins c-akt - metabolism, Rats, Sprague-Dawley, Reactive Oxygen Species - metabolism, Signal Transduction - drug effects, Stilbenes - pharmacology, p38 Mitogen-Activated Protein Kinases