Tanshinone II-A Is Protective against Human Umbilical Vein Endothelial Cell Injury after Exposure to Serum from Preeclampsia Patients

被引:5
|
作者
Wu, ChunFeng [1 ]
Yuan, Jing [1 ]
Sui, RenFang [2 ]
Li, ShuYuan [2 ]
Sun, JingXia [1 ]
机构
[1] Harbin Med Univ, Affiliated Hosp 1, Dept Obstet & Gynecol, Harbin 150010, Heilongjiang, Peoples R China
[2] Harbin Med Univ, Harbin 150010, Heilongjiang, Peoples R China
关键词
Preeclampsia; CD40/CD40; ligand; Tanshinone II-A; Human umbilical vein endothelial cells; MAGNESIUM-SULFATE THERAPY; HYDROGEN-PEROXIDE; EXPRESSION; HYPERTENSION; MANAGEMENT; MECHANISM; PREGNANCY; APOPTOSIS; ECLAMPSIA; STRESS;
D O I
10.1159/000363294
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Background/Aims: Preeclampsia (PE) is one of the most common and dangerous complications during pregnancy and is characterized by high blood pressure and significant amounts of protein in the urine. Vascular endothelial cell dysfunction is the major pathology in PE. This study was designed to assay the effects of tanshinone II-A (TII-A) on human umbilical vein endothelial cell (HUVEC) injury after incubation with serum from PE patients and to determine the underlying mechanism. Methods: After treating HUVECs with different TII-A concentrations, cell viability, apoptosis and CD40/CD40 ligand (CD40L) mRNA and protein expression levels were measured. Results: Incubation of HUVECs with serum from PE patients induced morphological alterations, caused decreased cell viability and increased the rate of apoptosis. However, TII-A (5-40 mu g/ml) significantly reversed these injuries. Importantly, preapplication of TII-A attenuated PE sera-induced expression of CD40 and CD40L mRNA and protein. Conclusion: TII-A has a protective effect against PE sera, likely through regulation of the CD40/CD40L signal transduction pathway. (C) 2014 S. Karger AG, Basel
引用
收藏
页码:101 / 108
页数:8
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