HMGB1
细胞凋亡
子痫前期
男科
内科学
内分泌学
血压
医学
化学
怀孕
生物化学
生物
炎症
遗传学
作者
Jiacui Zheng,Meirong Tian,Lanlan Liu,Xueqin Jia,Meiling Sun,Yongjing Lai
标识
DOI:10.1080/10641963.2021.2013492
摘要
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).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.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.MgSO4 reduces VEC apoptosis in PE rats via the miR-218-5p/HMGB1 pathway and thus plays a role in treating PE.
科研通智能强力驱动
Strongly Powered by AbleSci AI