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Association of the vascular endothelial damage and estrogen, progesterone / 대한산부인과학회지
Article in Ko | WPRIM | ID: wpr-41843
Responsible library: WPRO
ABSTRACT
OBJECTIVE: The aim of this study were to examine the serum level of estradiol, estriol, progesterone, oxidized LDL in preeclamtic patients and to evaluate the protective effects of estrogen and progesterone against lysophosphatidylcholine (LPC) induced cell death in Human umbilical vein endothelial cells (HUVECs). METHODS: We analysed the serum level of estradiol, estriol, progesterone, oxidized LDL in patients with preeclampsia and control. We used LPC to induce cell death in HUVECs. For cytotoxic assay, we did LDL assay for cell death and Resazurin assay for cell viability. HUVECs were exposed to various concentrations of LPC, LPC+estrogen, LPC+progesterone and we did cytotoxic assay. RESULTS: The serum estradiol, estriol were lower in the preeclamptic patients (P<0.05). Oxidized LDL were higher in the preeclamptic patients(P<0.05). LPC induced cell death in a concentration-dependant manner. Estrogen or progesterone inhibited LPC-induced cell death in a concentration-dependant manner (P<0.05). CONCLUSION: Estrogen and progesterone attenuated LPC-induced cytotoxicity. The results suggest that Oxidized LDL induced endothelial damage in preeclampsia may be induced by low serum estradiol, estriol and progesterone levels and prevented by estrogen and progesterone addition.
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Full text: 1 Index: WPRIM Main subject: Pre-Eclampsia / Progesterone / Lysophosphatidylcholines / Cell Survival / Cell Death / Estradiol / Estriol / Estrogens / Human Umbilical Vein Endothelial Cells Limits: Humans Language: Ko Journal: Korean Journal of Obstetrics and Gynecology Year: 2007 Type: Article
Full text: 1 Index: WPRIM Main subject: Pre-Eclampsia / Progesterone / Lysophosphatidylcholines / Cell Survival / Cell Death / Estradiol / Estriol / Estrogens / Human Umbilical Vein Endothelial Cells Limits: Humans Language: Ko Journal: Korean Journal of Obstetrics and Gynecology Year: 2007 Type: Article