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Sodium tanshinone IIA sulfonate prevents hypoxic trophoblast‐induced endothelial cell dysfunction via targeting HMGB1 release

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Preeclampsia (PE) is a serious blood pressure disorder of pregnancy. Systemic endothelial cell dysfunction, a hallmark of PE, is previously estimated to be induced by hypoxic trophoblast high mobility group… Click to show full abstract

Preeclampsia (PE) is a serious blood pressure disorder of pregnancy. Systemic endothelial cell dysfunction, a hallmark of PE, is previously estimated to be induced by hypoxic trophoblast high mobility group box 1 (HMGB1). In the present study, we investigated the protective effect of sodium tanshinone IIA sulfonate (STS), the soluble form of tanshinone IIA isolated from danshen, against hypoxic trophoblast HMGB1‐induced human umbilical vein endothelial cell (HUVEC) dysfunction. Our results showed that HMGB1 expression and release were significantly decreased in STS‐treated hypoxic JEG‐3 cells. A further study revealed hypoxic trophoblast HMGB1‐induced cytotoxicity and leukostasis of HUVEC as well as higher expression of cell adhesion molecules (VCAM‐1 and ICAM‐1) could be reversed by pretreatment with STS. In conclusion, our study suggests that STS is an effective agent against hypoxic trophoblast‐induced cell injury of HUVEC via targeting HMGB1 release and forms the basis of the development of such a compound in treating PE.

Keywords: dysfunction; endothelial cell; tanshinone iia; hypoxic trophoblast; trophoblast

Journal Title: Journal of Biochemical and Molecular Toxicology
Year Published: 2017

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