Magnesium sulfate reduces vascular endothelial cell apoptosis in rats with preeclampsia via the miR-218-5p/HMGB1 pathway

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.

KEYWORDS:

• Magnesium sulfate
• miR-218-5p
• high-mobility group protein b1
• preeclampsia
• rats

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by The Teachers’ research of Jining Medical University (No.JYFC2019FKJ174).