Tanshinone IIA Inhibits Tissue Factor Expression Induced by Thrombin in Human Umbilical Vein Endothelial Cells via PAR-1 and p38 MAPK Signaling Pathway

凝血酶 脐静脉 p38丝裂原活化蛋白激酶 化学 MAPK/ERK通路 分子生物学 NADPH氧化酶 组织因子 信号转导 活性氧 生物 内科学 生物化学 医学 血小板 体外 凝结
作者
Zewen Zhang,Daming Xu,Wenjun Yu,Jinfeng Qiu,Chengwei Xu,Chunling He,Xian-Ru Xu,Jun Yin
出处
期刊:Acta Haematologica [Karger Publishers]
卷期号:145 (5): 517-528 被引量:3
标识
DOI:10.1159/000525055
摘要

<b><i>Background:</i></b> The potential signaling pathway of TSA suppressing TF expression induced by thrombin was unknown. Thus, the transcription of TF in HUVECs and the expressions of DCF, phospho-p38 MAPK, NADPH oxidase 4, PAR-1, and NF-κB were detected in our study. <b><i>Methods:</i></b> HUVECs were randomly divided into control group, thrombin-treated group (with 5 U/mL of thrombin), and 4 TSA-treated groups (with 5 U/mL of thrombin plus TSA with 4 different concentrations of 1 μg/mL, 10 μg/mL, 100 μg/mL, and 1 mg/mL, respectively). <b><i>Results:</i></b> After incubation with thrombin for 6 h at 37°C, the results showed increased TF mRNA, TF procoagulant activity, and antigen of TF in HUVECs of thrombin-treated group (<i>p</i> &#x3c; 0.01); however, they were restored by TSA in a dose-dependent manner (<i>p</i> &#x3c; 0.01). In addition, reactive oxygen species (ROS), phospho-p38 MAPK, NADPH oxidase 4, NF-κB, and PAR-1 expressed more intensively, and phosphorylated Akt decreased obviously in HUVECs after thrombin stimulation (<i>p</i> &#x3c; 0.01); however, they were reversed to different extents by TSA in a dose-dependent manner (<i>p</i> &#x3c; 0.01). <b><i>Conclusions:</i></b> Study suggests that TSA inhibits TF expression induced by thrombin in cultured HUVECs, and the potential signaling pathway of which is TSA interrupts the activation of PAR-1 and NADPH oxidase as well as derivative ROS generation, thereafter suppresses the activation of NF-κB, the upstream signal molecule of TF, via hampering phosphorylation of p38 MAPK and dephosphorylation of Akt, and finally inhibits thrombin-induced TF overexpression.
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