Cardamonin inhibits angiotensin II-induced vascular smooth muscle cell proliferation and migration by downregulating p38 MAPK, Akt, and ERK phosphorylation

• DOI: 10.1007/s11418-014-0825-0
• Publication Date: 2014-03-04T08:46:50Z
• Authors: Yan-Jing Shen; Xue-Xin Zhu; Xian Yang; Bo Jin; Jin-Jian Lu; Bin Ding; Zhi-Shan Ding; Su-Hong Chen
• Keywords: 0301 basic medicine; Angiotensin II; Myocytes, Smooth Muscle; Down-Regulation; p38 Mitogen-Activated Protein Kinases; Muscle, Smooth, Vascular; Rats; 3. Good health; Rats, Sprague-Dawley; 03 medical and health sciences; Chalcones; Cell Movement; Animals; Enzyme Inhibitors; Phosphorylation; Extracellular Signal-Regulated MAP Kinases; Proto-Oncogene Proteins c-akt; Cells, Cultured; Cell Proliferation

Cardamonin is a chalconoid isolated from various herbs, such as Alpinia katsumadai and Carya cathayensis Sarg. This study examined the effect of cardamonin on angiotensin II (Ang II)-induced proliferation and migration in rat vascular smooth muscle cells (VSMCs) as well as its underlying mechanisms. The results showed that cardamonin significantly inhibited Ang II-induced proliferation and migration in rat VSMCs in a concentration-dependent manner. Moreover, cardamonin suppressed Ang II-induced phosphorylation of p38 MAPK, Akt, and extracellular regulated protein kinase (ERK). These findings indicate that the downregulation of p38 MAPK, Akt, and ERK phosphorylation might be, at least in part, involved in cardamonin-suppressed proliferation and migration induced by Ang II in rat VSMCs. As proliferation and migration of VSMCs play critical roles in the pathogenesis of atherosclerosis, cardamonin might be a potential candidate for atherosclerosis treatment.