Magnesium sulfate reduces vascular endothelial cell apoptosis in rats with preeclampsia via the miR-218-5p/HMGB1 pathway. (17th February 2022)

• Record Type: Journal Article
• Authors: Zheng, Jiacui; Tian, Meirong; Liu, Lanlan; Jia, Xueqin; Sun, Meiling; Lai, Yongjing
• Is Part Of: Clinical and experimental hypertension. Volume 44:Number 2(2022)
• Page Start: 159
• Page End: 166
• Publication Date: 2022-02-17
• Subjects: Magnesium sulfate -- miR-218-5p -- high-mobility group protein b1 -- preeclampsia -- rats; Hypertension -- Chemotherapy -- Periodicals; Hypotensive agents -- Periodicals; 616.132
• DOI: 10.1080/10641963.2021.2013492
• Languages: English
• ISSNs: 1064-1963

Abstract

ABSTRACT: 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 14 th 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 11 th, 13 th, 15 th, 17 th, and 19 th 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.