Abstract Title:

Astragaloside IV inhibits PMA-induced EPCR shedding through MAPKs and PKC pathway.

Abstract Source:

Immunopharmacol Immunotoxicol. 2017 Jun ;39(3):148-156. Epub 2017 Apr 3. PMID: 28367652

Abstract Author(s):

Yu Ma, Yi Zhao, Ran Zhang, Xiaoxia Liang, Zhongqiong Yin, Yi Geng, Gang Shu, Xu Song, Yuanfeng Zou, Lixia Li, Lizi Yin, Guizhou Yue, Yinglun Li, Gang Ye, Changliang He

Article Affiliation:

Yu Ma


Astragaloside IV (AS-IV), a main active substance isolated from Astragalus membranaceus Bunge, has been shown to have multiple pharmacological effects. Endothelial cell protein C receptor (EPCR) is a marker of inflammation, and is also a major member of protein C (PC) anti-coagulation system. EPCR can be cut off from the cell surface by tumor necrosis factor-α converting enzyme (TACE), which is controlled through mitogen-activated protein kinase (MAPK) and protein kinase C (PKC) pathways. To develop novel therapeutic drug for EPCR shedding, the effect of AS-IV was studied in phorbol-12-myristate 13-acetate (PMA)-induced human umbilical vein endothelialcells (HUVECs) and the potential molecular mechanism of AS-IV action was investigated. The results showed that AS-IV could significantly inhibit PMA-induced EPCR shedding. In further study, AS-IV suppressed the expression and activity of TACE. In addition, AS-IV could decrease the phosphorylation of MAPK such as janus kinase (JNK) and p38, and inhibit activation of PKC through the prevention of non-phosphorylation and phosphorylation of specific PKC isoforms in PMA-stimulated HUVECs. These findings indicate that AS-IV may be used as a natural medicine to treat EPCR-related systemic inflammation and cardiovascular diseases by targeting MAPK and PKC pathway.

Study Type : In Vitro Study

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