Abstract:

Ｏｂｊｅｃｔｉｖｅ：To investigate the effect and possible mechanism of pioglitazon on the calcification of rat vascular smooth muscle cells (VSMCs) in vitro.
Ｍｅｔｈｏｄｏｌｏｇｙ：βglycerophosphate (10 mmol/L) was used to induce the calcification of VSMCs, with different concentrations (5 μmol/L、10 μmol/L、15 μmol/L、20 μmol/L) of PIO to intervene for 12d. The calcium deposits were tested by Alizarin red staining. The extracellular calcium content was detected by Calcium Assay Kit. Western Blot was used to measure the expressions of αsmooth muscle actin (αSMA), runtrelated transcription factor 2 (Runx2), bone morphogenetic protein 2 (BMP2), βcatenin, GSK3β, pGSK3β and cyclinD1. On the basis of 10 mmol/L βglycerophosphate and 20 μmol/L PIO, 20 μmol/L PPARγ antagonist GW9662 was added to the cell culture media. The changes of the above indexes were observed.
Ｒｅｓｕｌｔｓ：（1) The calcium content in calcification group was increased significantly compared with that in controls (P<005), and all different concentrations of PIO could reduced extracellular calcium content (P<005). Alizarin red staining was strong positive in calcified VSMCs, and PIO (20 μmol/L) intervention group was almost negative. （2) The expressions of Runx2, βcatenin, pGSK3β, BMP2 and cyclinD1 were increased significantly in calcification group, and 20 μmol/L PIO group obviously downregulated the expressions of all the above proteins, while upregulated the expression of αSMA. （3) PPARγ antagonist GW9662 could partly block the effect of PIO on calcified VSMCs.
Ｃｏｎｃｌｕｓｉｏｎ：PPARγ agonist PIO can alleviate rat aortic VSMCs calcification induced by βglycerophosphate via inhibiting the activity of Wnt/βcatenin signaling pathway.

Key words: peroxisome proliferatoractivated receptor gamma,vascular smooth muscle cells,calcificationWnt/&beta, -catenin signaling pathway