Grape Seed Procyanidin B2 Inhibits Human Aortic Smooth Muscle Cell Proliferation and Migration Induced by Advanced Glycation End Products

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  • CAI Qian
    Key Laboratory of Cardiovascular Proteomics of Shandong Province, Department of Geriatrics, Qi-Lu Hospital of Shandong University
  • LI Bao-ying
    Key Laboratory of Cardiovascular Proteomics of Shandong Province, Department of Geriatrics, Qi-Lu Hospital of Shandong University
  • GAO Hai-qing
    Key Laboratory of Cardiovascular Proteomics of Shandong Province, Department of Geriatrics, Qi-Lu Hospital of Shandong University
  • ZHANG Jian-hua
    Institute of Basic Science, Medical Science Academy of Shandong
  • WANG Jun-fu
    Institute of Basic Science, Medical Science Academy of Shandong
  • YU Fei
    Key Laboratory of Cardiovascular Proteomics of Shandong Province, Department of Geriatrics, Qi-Lu Hospital of Shandong University
  • YIN Mei
    Key Laboratory of Cardiovascular Proteomics of Shandong Province, Department of Geriatrics, Qi-Lu Hospital of Shandong University
  • ZHANG Zhen
    Key Laboratory of Cardiovascular Proteomics of Shandong Province, Department of Geriatrics, Qi-Lu Hospital of Shandong University

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Advanced glycation end product (AGE)-induced vascular smooth muscle cell (VSMC) proliferation is vital to the progression of diabetic vasculopathy. A grape seed procyanidin extract has been reported to possess anti-oxidative and anti-inflammatory properties and to display a significant cardiovascular protective effect, but little is know about the underlying mechanism. The objective of this present study was to determine whether GSPB2 (grape seed procyanidin B2), which is a dimeric procyanidin and more biologically active, could inhibit AGE-induced VSMC proliferation by affecting the production of ubiquitin COOH-terminal hydrolase 1 (UCH-L1), the degradation of IκB-α and nuclear translocation of NF-κB in human aortic smooth muscle cells (HASMCs). Our data show that GSPB2 preincubation markedly inhibited AGE-induced proliferation and migration of HASMCs in a dose-dependent manner and upregulated the protein level of UCH-L1. Further studies revealed that the GSPB2 pretreatment markedly attenuated the degradation of IκB-α and nuclear translocation of NF-κB by modulating ubiquitination of IκB-α in AGE-exposed HASMCs. These results collectively suggest that AGE-induced HASMC proliferation and migration was suppressed by GSPB2 through regulating UCH-L1 and ubiquitination of IκB-α. GSPB2 may therefore have therapeutic potential in preventing and treating vascular complications of diabetes mellitus.

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