Anti-proliferative Effect of Licochalcone A on Vascular Smooth Muscle Cells

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  • Park Jin-Hee
    Division of Cardiovascular and Rare Diseases, Center for Biomedical Sciences, NIH
  • Lim Hyun Joung
    Division of Cardiovascular and Rare Diseases, Center for Biomedical Sciences, NIH
  • Lee Kuy-Sook
    Division of Cardiovascular and Rare Diseases, Center for Biomedical Sciences, NIH
  • Lee Seahyoung
    Division of Cardiovascular and Rare Diseases, Center for Biomedical Sciences, NIH
  • Kwak Hyun-Jeong
    Division of Cardiovascular and Rare Diseases, Center for Biomedical Sciences, NIH
  • Cha Jeong-Heon
    Department of Oral Biology, BK21 Project, Oral Science Research Center, Yonsei University College of Dentistry
  • Park Hyun-Young
    Division of Cardiovascular and Rare Diseases, Center for Biomedical Sciences, NIH

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説明

Licochalcone A, a flavonoid found in licorice root (Glycyrrhiza glabra), is known for its anti-microbial activity and its reported ability to inhibit cancer cell proliferation. In the present study, we investigated whether licochalcone A inhibits rat vascular smooth muscle cell (rVSMC) proliferation. Our data indicate that 5 μM licochalcone A inhibited platelet-derived growth factor (PDGF)-induced rVSMC proliferation, possibly through its ability to block the progression of the cell cycle from G1 to S phase. In addition, 5 μM licochalcone A significantly inhibited the PDGF-induced expression of cyclin A, cyclin D1, CDK2, and CDK4, and the phosphorylation of Rb. Licochalcone A also reversed the decrease in p27kip1 expression reduced by PDGF. Finally, licochalcone A inhibited the PDGF-induced activation of extracellular signal-regulated kinase (ERK)1/2. Together, these data provide the first evidence that licochalcone A can regulate rVSMC proliferation and suggest that licochalcone A inhibits the proliferation of rVSMCs by suppressing the PDGF-induced activation of the ERK1/2 pathway and Rb phosphorylation, resulting in cell cycle arrest.

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