Baicalin enhances the proliferation and invasion of trophoblasts and suppresses vascular endothelial damage by modulating long non‐coding RNA NEAT1/miRNA‐205‐5p in hypertensive disorder complicating pregnancy

Aim Trophoblastic and vascular endothelial injuries were closely associated with the pathogenesis of hypertensive disorder complicating pregnancy (HDCP). The present study was designed to determine the functional role of baicalin in the proliferation and invasion of trophoblasts and vascular endothelial injury. Methods Ang II was adopted to stimulate HTR‐8/SVneo and human umbilical vein endothelial cells (HUVECs). Cell viability was examined by CCK‐8 assay. Flow cytometry and TUNEL staining determined cell apoptosis. Invasive ability of HTR‐8/SVneo cells was measured by transwell assay. In vitro angiogenesis of HUVECs was assessed by Tube formation assay. In addition, the production of reactive oxygen species (ROS) was determined by DCFH‐DA staining. Furthermore, long non‐coding RNA (lncRNA) NEAT1 and miRNA‐205‐5p levels were detected using real‐time quantitative polymerase chain reaction and the binding relationship between lncRNA NEAT1 and miRNA‐205‐5p was verified by dual‐luciferase reporter assay. Moreover, interactions among lncRNA NEAT1, miRNA‐205‐5p, and MMP9 or vascular endothelial growth factor (VEGF) were confirmed by RNA immunoprecipitation assay. Results Baicalin visibly improved cell viability, reduced the apoptosis of Ang II‐stimulated HTR‐8/SVneo and HUVEC cells, and repressed overproduction of ROS. Additionally, baicalin promoted the invasion of Ang II‐stimulated HTR‐8/SVneo cells and induced a stronger in vitro angiogenesis of Ang II‐stimulated HUVECs. What's more, baicalin upregulated lncRNA NEAT1 expression and downregulated miR‐205‐5p expression. LncRNA NEAT1 sponged miR‐205‐5p and inhibited the combination of miR‐205‐5p and MMP9 or VEGF. Conclusions Baicalin can facilitate the proliferation and invasion of trophoblasts and alleviate vascular endothelial damage by upregulating lncRNA NEAT1 to impede the interaction between miR‐205‐5p and MMP9 or VEGF.