Agastache rugosa Kuntze extract, containing the active component rosmarinic acid, prevents atherosclerosis through up-regulation of the cyclin-dependent kinase inhibitors p21WAF1/CIP1 and p27KIP1

- A. rugosa extract inhibited PDGF-BB-stimulated VSMC proliferation and DNA synthesis.
- A. rugosa extract caused arrest of the cell cycle at the G0/G1 transition.
- The cell cycle arrest was caused by up-regulating the levels of CKIs.
- Among the components, RA only inhibited DNA synthesis and PCNA expression.

Agastache rugosa (Fisch. & C.A. Mey.) Kuntze (A. rugosa), commonly known as Korean mint, has traditionally been used for both food and medicine, depending on which part of the plant is used. We investigated the anti-proliferative activities of A. rugosa extract in vascular smooth muscle cells (VSMCs) and analysed several molecular pathways to determine the active component of the extract. A. rugosa extract inhibited PDGF-BB-stimulated VSMC proliferation and DNA synthesis. A. rugosa extract caused arrest of the cell cycle at the G0/G1 transition by up-regulating the levels of p21WAF1/CIP1 and p27KIP1. Among the components of the A. rugosa extract reported in a previous study, rosmarinic acid (RA) only inhibited DNA synthesis and dose-dependently suppressed PCNA expression. These results indicate that A. rugosa extract, which includes the active component RA, demonstrates anti-proliferative activity by arresting the cell cycle at the G0/G1 phase through the upregulation of p21WAF1/CIP1 and p27Kip1 expression.