Magnesium sulfate reduces vascular endothelial cell apoptosis in rats with preeclampsia via the miR-218-5p/HMGB1 pathway
Autor: | Jiacui Zheng, Meirong Tian, Lanlan Liu, Xueqin Jia, Meiling Sun, Yongjing Lai |
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Jazyk: | angličtina |
Rok vydání: | 2022 |
Předmět: | |
Zdroj: | Clinical and Experimental Hypertension, Vol 44, Iss 2, Pp 159-166 (2022) |
Druh dokumentu: | article |
ISSN: | 1064-1963 1525-6006 10641963 |
DOI: | 10.1080/10641963.2021.2013492 |
Popis: | Objective This study aims to investigate the mechanism by which magnesium sulfate regulates the miR-218-5p/HMGB-pathway-mediated apoptosis of vascular endothelial cells (VECs) in rats with preeclampsia (PE). Methods Twenty pregnant rats were randomly divided into four groups: normal, PE, MgSO4, and high-mobility group protein B1 (HMGB1)-agomir groups. On the 14th day of each rat’s pregnancy, endotoxin was used to establish a PE model in the PE, MgSO4, and HMGB1-agomir groups. Then, the MgSO4 and HMGB1-agomir groups were treated with magnesium sulfate. Finally, HMGB1 overexpression was performed only in the HMGB1-agomir group. The rats’ urinary protein content and systolic blood pressure at 24 h were detected on the 11th, 13th, 15th, 17th, and 19th day of pregnancy. Results Compared with the PE group, 24-h urinary protein content, blood pressure, VEC apoptosis rate, apoptosis marker levels, and HMGB1 expression decreased while miR-218-5p levels increased in the MgSO4 group. The dual-luciferase assay revealed that HMGB1 can be targeted and regulated by miR-218-5p. Compared with the MgSO4 group, 24-h urinary protein content, blood pressure, VEC apoptosis rate, apoptosis marker levels, and HMGB1 expression increased while miR-218-5p levels decreased in the HMGB1-agomir group. Conclusion MgSO4 reduces VEC apoptosis in PE rats via the miR-218-5p/HMGB1 pathway and thus plays a role in treating PE. |
Databáze: | Directory of Open Access Journals |
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