血管平滑肌细胞vascularsmoothmusclecellsvsmc是动脉粥样.docVIP

Hydroxysafflor yellow A suppresses oxidized low density lipoprotein induced proliferation of vascular smooth muscle cells Lin Sheng*, Shaojie Bi, Chao Cheng, Jingbo Zhang Department of cardiovascular, The 2nd affiliated Hospital, Jinan, Shandong 250033, China *Correspondence: Dr. Lin Sheng, Department of cardiovascular, The 2nd affiliated Hospital, Jinan, Shandong 250033, China; Email: sandraeller@163.com ? Abstract To investigate the relationship between the suppression of Hydroxysafflor yellow A (HSYA) on the oxidized low density lipoprotein (ox-LDL) induced proliferation of vascular smooth muscle cells (VSMCs) and the mRNA and protein expression of extracellular signal-regulated protein kinase 1/2 (ERK1/2) and mitogen activated protein kinase phospholipase-1 (MAKP-1), VSMCs were treated with HSYA at 10 μmol/L and/or ox-LDL at 35 mg/L for 48 h. MTT assay was done to measure cell survival rate, flow cytometry to detect cell cycle, reverse transcription PCR and Western blot to detect the expression of ERK1/2 and MAKP-1. When compared to cells treated with ox-LDL alone, the survival rate of cells treated with two reagents was reduced and the proportion of cells in G0/G1 phase significantly increased, with increased MKP-1 expression. The study suggests HSYA can inhibit VSMC proliferation via increasing MKP-1 expression, reducing p-ERK1/2 activity and suppressing cell cycle. Key words: Hydroxysafflor yellow A; oxidized low density lipoprotein, ERK1/2, MAKP-1, smooth muscle cells Introduction Proliferation of vascular smooth muscle cells (VSMCs) is a shared pathological basis in atherosclerosis, hypertension and vascular restenosis after interventional treatment (Curcio et al., 2011). Oxidized low-density lipoproteins (ox-LDL) can cause damage to VSMCs, stimulate the proliferation of VSMCs and induce their apoptosis. This may reduce the stability of atheromatous plaques, and plays an important role in the occurrence and development of vascular lesions (Stoll and