Effect of emodin on the proliferation and migration of hypoxia pulmonary artery smooth muscle cells

Abstract

Objective To observe the inhibitory effect of emodin on the proliferation and migration of pulmonary artery smooth muscle cells. Methods Primary cultured human pulmonary arterial smooth muscle cells (HPASMC) were cultured in a routine manner to establish an hypoxic cell model. Emodin at different concentrations (0, 5, 10, 15 and 20 μmol/L) 48 and 72 h later, the proliferation and migration of hypoxic pulmonary artery were detected by methyl thiazol tetrazolium (MTT) assay and Transwell invasion assay. Western blotting assay was used to determine the expression of p38 protein in hypoxia HPASMC induced by emodin. Results Emodin inhibited the proliferation and migration of hypoxic HPASMC in a time-and concentration-dependent manner. When the concentration was 20 μmol/L, the effect was the most significant, and the inhibitory rates at 12, 24, 48 and 72 h were (53.46±1.81)%, (61.32±2.69)%, (76.34±3.05)% and (84.43±3.18)%, respectively. (68.90±8.49), (46.10±5.63), (27.56±5.38) in the Transwell experimental group (5, 10, 15 and 20 μmol/[(12.61±3.68)] compared with the control group [(88.59±8.56)]. Compared with the control group, the experimental group p38 protein expression was reduced (P=0.001). Conclusion Emodin can significantly inhibit the proliferation and migration of human pulmonary artery smooth muscle cells under hypoxic conditions and down-regulate the expression of p38 protein. Key words: Emodin; Pulmonary artery smooth muscle cells; Proliferation; Migration