The effect of ginsenoside Rk1 in junctional protein of severe preeclamptic placenta.
- Author:
Seung Chul LIM
1
;
Yong Sun MAENG
;
Ja Young KWON
;
Myoung Hwa KANG
;
Jeong Hye HYANG
;
Young Han KIM
;
Young Keun KWON
;
Yong Won PARK
Author Information
1. Department of Obstetrics and Gynecology, Yonsei University Health System, Seoul, Korea. ywparkob@yuhs.ac
- Publication Type:Original Article
- Keywords:
Placenta;
Preeclampsia;
Intrauterine growth restriction;
Junctional protein;
Ginsenoside Rk1
- MeSH:
Anoxia;
Blotting, Western;
Cesarean Section;
Endothelial Cells;
Endothelium;
Female;
Fetal Development;
Fetal Growth Retardation;
gamma Catenin;
Ginsenosides;
Humans;
Immunohistochemistry;
Occludin;
Placenta;
Pre-Eclampsia;
Pregnancy;
Proteins
- From:Korean Journal of Obstetrics and Gynecology
2009;52(3):301-308
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: To investigate the differential expression of junctional proteins in the normal and preeclamptic human placenta and the effect of ginsenoside Rk1 in junctional proteins. METHODS: Placental tissues from 10 women with severe preeclampsia and 5 normal women were collected at the time of their cesarean section. Five of 10 preeclamptic women were complicated with intrauterine growth restriction (IUGR). Immunohistochemistry and Western blotting was employed to localize junctional proteins (zo-1, occludin and plakoglobin) positive cells. The placental explant culture was performed to investigate if Rk1 can attenuate the expression of junctional proteins (zo-1, occluding and plakoglobin) induced by deferoxamine-induced hypoxia. Rk1 was treated at the day 3 and Western blot analysis was performed for protein quantification. RESULTS: There was no different expression of zo-1 and plakoglobin among all the study groups. Occludin showed negative at the endothelial cells of the terminal villi in both normal and preeclampsia groups. At the endothelial cells of the stem villi, occludin was detected in both normal and severe preeclamptic placenta with normal fetal growth. However, severe preeclampsia with IUGR were decreased expression of occludin at the endothelial cells of the stem villi. When we administered Rk1 to the placenta treated with DFO, expression of occludin was not different. CONCLUSION: The placental expression of zo-1 and plakoglobin were not different among the study groups, while that of occludin was significantly decreased at the endothelium of stem villi in severe preeclampsia with IUGR. Rk-1 showed no effect on the placental junctional proteins. These results suggest that occludin may play a role in pathophysiology of fetal growth restriction in utero.
