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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Hou, Junran Ye, Songshan Yang, Lei Mao, Bingyu Fu, Weiyun |
| Description | Author Affiliation: Ye S ( Department of Medical Experimental Center, Zhang Zhongjing Traditional Chinese Medicine College, Nanyang Institute of Technology, Nanyang, Henan 473004, P.R. China.); Mao B ( Department of Medical Experimental Center, Zhang Zhongjing Traditional Chinese Medicine College, Nanyang Institute of Technology, Nanyang, Henan 473004, P.R. China.); Yang L ( Department of Medical Experimental Center, Zhang Zhongjing Traditional Chinese Medicine College, Nanyang Institute of Technology, Nanyang, Henan 473004, P.R. China.); Fu W ( Department of Medical Experimental Center, Zhang Zhongjing Traditional Chinese Medicine College, Nanyang Institute of Technology, Nanyang, Henan 473004, P.R. China.); Hou J ( Department of Medical Experimental Center, Zhang Zhongjing Traditional Chinese Medicine College, Nanyang Institute of Technology, Nanyang, Henan 473004, P.R. China.) |
| Abstract | Paeoniflorin, the major component of Paeonia lactiflora pall, has previously been reported to prevent thrombosis. Plasminogen activator urokinase (uPA) is a serine protease that markedly facilitates normal thrombosis resolution. Paeoniflorin and uPA have been linked to the mitogenactivated protein kinase (MAPK) signaling pathway. In the current study, the influence of paeoniflorin on the expression of uPA was investigated and the underlying regulatory mechanism was preliminarily determined. The prothrombotic state of the model animals treated with paeoniflorin were assessed by enzymelinked immunosorbent assay (ELISA). Additionally, the cytotoxicity of paeoniflorin on human umbilical vein endothelial cell (HUVEC) cultures was estimated using a methyl thiazolyl tetrazolium assay and the possible pathways involved in the interaction between paeoniflorin and uPA were evaluated using western blot analysis. The ELISA results demonstrated that the levels of 6keto prostaglandin F1a, fibronectin and uPA were significantly upregulated by treatment with paeoniflorin compared with control (P<0.05). By contrast, the expression of fibrinogen, Ddimer and thromboxane B2 were inhibited. With an increase in the concentration of paeoniflorin the cell viability of HUVECs decreased gradually. The results of western blot analysis demonstrated that paeoniflorin increased the phosphorylation of MAPK 14 (p38) and MAPK 8 (JNK). The present study demonstrated that paeoniflorin has the potential to improve the prethrombotic state and recanalize thrombosis by increasing the expression of uPA, which may be mediated via regulation of the p38 and JNK MAPK signaling pathways. However, this treatment effect was dependent on the concentration of paeoniflorin used, an unsuitable concentration of the agent would result in a negative effect on the antithrombosis pathways. |
| ISSN | 17912997 |
| e-ISSN | 17913004 |
| DOI | 10.3892/mmr.2016.5146 |
| Journal | Molecular Medicine Reports |
| Issue Number | 6 |
| Volume Number | 13 |
| Language | English |
| Publisher | Spandidos Publications |
| Publisher Date | 2016-06-01 |
| Publisher Place | Greece |
| Access Restriction | Open |
| Subject Keyword | Discipline Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology |
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