Why the study?
Does sodium tanshinone IIA sulfonate prevent hypoxic trophoblast-induced endothelial cell dysfunction in a preclinical model of preeclampsia?
Does sodium tanshinone IIA sulfonate prevent hypoxic trophoblast-induced endothelial cell dysfunction in a preclinical model of preeclampsia?
Sodium tanshinone IIA sulfonate protects against hypoxic trophoblast-induced endothelial dysfunction in vitro, highlighting its potential as a therapeutic agent for preeclampsia.
STS may mitigate endothelial dysfunction in preeclampsia cell models; leaves open clinical translation.
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.
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Zhao et al. (2017) studied this question.
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