Mechanism of ligustrazini against thrombosis |
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Authors: | Song J Ruan Q |
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Institution: | Department of Infectious Disease, Tongji Hospital, Tongji Medical University, Wuhan 430030, China;Department of Pathology, Tongji Medical University, Wuhan 430030, China |
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Abstract: | 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-kappa B) 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. |
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Keywords: | ligustrazini thrombosis mechanism |
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