Zhao Min, Feng Yaling, Xiao Jianping, Liang Jie, Yin Yongxiang, Chen Daozhen
Department of Obstetrics & Gynecology, Wuxi Maternity and Child Health Hospital Affiliated Nanjing Medical University, Wuxi, 214002, People's Republic of China.
Department of Pathology, Wuxi Maternity and Child Health Hospital Affiliated Nanjing Medical University, Wuxi, 214002, People's Republic of China.
J Biochem Mol Toxicol. 2017 Jul;31(7). doi: 10.1002/jbt.21903. Epub 2017 Feb 16.
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.
子痫前期（PE）是一种严重的妊娠期血压紊乱疾病。全身内皮细胞功能障碍是PE的一个标志，此前估计是由缺氧滋养细胞高迁移率族蛋白B1（HMGB1）诱导所致。在本研究中，我们研究了丹参酮IIA磺酸钠（STS）——从丹参中分离出的丹参酮IIA的可溶形式——对缺氧滋养细胞HMGB1诱导的人脐静脉内皮细胞（HUVEC）功能障碍的保护作用。我们的结果表明，在经STS处理的缺氧JEG - 3细胞中，HMGB1的表达和释放显著降低。进一步的研究表明，缺氧滋养细胞HMGB1诱导的HUVEC细胞毒性和白细胞淤滞以及细胞黏附分子（VCAM - 1和ICAM - 1）的高表达可通过STS预处理得以逆转。总之，我们的研究表明，STS是一种通过靶向HMGB1释放来对抗缺氧滋养细胞诱导的HUVEC细胞损伤的有效药物，并为开发此类化合物治疗PE奠定了基础。
