Plasminogen activator inhibitor 1 (PAI 1) is one of important coagulant factors. Endotoxin lipopolysaccharide (LPS) induces thrombosis by stimulating PAI 1 secretion of vascular cells (EC). Using sandwich enzyme li...Plasminogen activator inhibitor 1 (PAI 1) is one of important coagulant factors. Endotoxin lipopolysaccharide (LPS) induces thrombosis by stimulating PAI 1 secretion of vascular cells (EC). Using sandwich enzyme linked immunosorbent assay (ELISA) and Northern blot, was investigated the effects of Chinese medicine ligustrazini on PAI 1 expression in EC and LPS stimulated EC. The results showed that ligustrazini inhibited both basal and LPS induced PAI 1 mRNA expression in EC. The effect of ligustrazini on LPS induced PAI 1 secretion worked in a dose dependent manner. This study provided theoretic and experimental evidence for use of ligustrazini against septic shock and cardiovascular diseases.展开更多
Objective To investigate the mechanism of Chinese medicine ligustrazini against thrombosis, and the effects of ligustrazini on plasminogen activator inhibitor (PAI 1) expression in normal endothelial cells and lipop...Objective To investigate the mechanism of Chinese medicine ligustrazini against thrombosis, and the effects of ligustrazini on plasminogen activator inhibitor (PAI 1) expression in normal endothelial cells and lipopolysaccharide (LPS) stimulated endothelial cells Methods Human umbilical vein endothelial cells (HUVECs) were cultured by trypsin digestion method PAI 1 protein in HUVEC conditioned medium was measured by Sandwich enzyme linked immunosorbent assay (ELISA), and PAI 1 mRNA expression was determined by Northern blot analysis Using electrophoretic mobility shift assay (EMSA), we observed HUVEC nuclear factor kappa B (NF κB) nuclear translocation Results LPS treatment of cultured HUVECs resulted in a significant increase in PAI 1 protein and mRNA expression by these cells However, when HUVECs were incubated with LPS plus ligustrazini, the upregulation of PAI 1 by LPS was abated Moreover, ligustrazini could decrease the basal level of PAI 1 protein and mRNA in HUVECs as compared with control Nuclear extracts prepared from HUVECs stimulated by LPS demonstrated that binding to the NF kB oligo nucleotide increased as compared with the unstimulated cells, but ligustrazini did not change those binding in the absence or presence of LPS Conclusions Ligustrazini inhibited both basal and LPS induced PAI 1 protein and mRNA expression in endothelial cells, and the modulation of PAI 1 in HUVECs by ligustrazini might have other mechanisms rather than NF kB pathway展开更多
基金the grant from NationalNatural Sciences Foundation of China(No. 39730 2 2 0 )
文摘Plasminogen activator inhibitor 1 (PAI 1) is one of important coagulant factors. Endotoxin lipopolysaccharide (LPS) induces thrombosis by stimulating PAI 1 secretion of vascular cells (EC). Using sandwich enzyme linked immunosorbent assay (ELISA) and Northern blot, was investigated the effects of Chinese medicine ligustrazini on PAI 1 expression in EC and LPS stimulated EC. The results showed that ligustrazini inhibited both basal and LPS induced PAI 1 mRNA expression in EC. The effect of ligustrazini on LPS induced PAI 1 secretion worked in a dose dependent manner. This study provided theoretic and experimental evidence for use of ligustrazini against septic shock and cardiovascular diseases.
文摘Objective To investigate the mechanism of Chinese medicine ligustrazini against thrombosis, and the effects of ligustrazini on plasminogen activator inhibitor (PAI 1) expression in normal endothelial cells and lipopolysaccharide (LPS) stimulated endothelial cells Methods Human umbilical vein endothelial cells (HUVECs) were cultured by trypsin digestion method PAI 1 protein in HUVEC conditioned medium was measured by Sandwich enzyme linked immunosorbent assay (ELISA), and PAI 1 mRNA expression was determined by Northern blot analysis Using electrophoretic mobility shift assay (EMSA), we observed HUVEC nuclear factor kappa B (NF κB) nuclear translocation Results LPS treatment of cultured HUVECs resulted in a significant increase in PAI 1 protein and mRNA expression by these cells However, when HUVECs were incubated with LPS plus ligustrazini, the upregulation of PAI 1 by LPS was abated Moreover, ligustrazini could decrease the basal level of PAI 1 protein and mRNA in HUVECs as compared with control Nuclear extracts prepared from HUVECs stimulated by LPS demonstrated that binding to the NF kB oligo nucleotide increased as compared with the unstimulated cells, but ligustrazini did not change those binding in the absence or presence of LPS Conclusions Ligustrazini inhibited both basal and LPS induced PAI 1 protein and mRNA expression in endothelial cells, and the modulation of PAI 1 in HUVECs by ligustrazini might have other mechanisms rather than NF kB pathway