Archives of Medical Science (Feb 2020)

Mechanisms underlying the improvement of preeclampsia through salvianolic acid B-regulated miRNA-155/CXCR4

  • Chuanlian Zhang,
  • Xue Han,
  • Xiaoxue Wang

DOI
https://doi.org/10.5114/aoms.2020.92938
Journal volume & issue
Vol. 19, no. 2
pp. 430 – 447

Abstract

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Introduction The aim of this study was to evaluate the effects and mechanisms of salvianolic acid B (Sal B) in preeclampsia treatment by in vivo and in vitro study. Material and methods Rats were randomly divided into 5 groups. In order to establish the model of preeclampsia, endotoxin was administered to the rats in the Sal B intervention and model groups. The systolic blood pressure (SBP) of the tail artery and urine protein concentration were observed at different points, the miRNA-155 and CXCR4 gene expression levels by RT-PCR and the CXCR4 and p-AKT protein expression by WB assay. Using HTR8/SVneo to explain the mechanisms; evaluating the miRNA-155 and CXCR4 mRNA expression by RT-PCR assay, measuring the cell invasion and migration by transwell and wound healing assay in different groups; evaluating the CXCR4 and p-AKT protein expression by WB assay and p-AKT nucleation volume by cellular immunofluorescence were evaluated. Results Compared with the normal group, the systolic blood pressure and urine protein were significantly increased in the model group (p < 0.05), serum NO concentration was significantly down-regulated (all p < 0.05), CXCR4 and miRNA-155 mRNA expression was significantly different and CXCR4 and p-AKT protein expression was significantly suppressed (all p < 0.05). With Sal B supplement, the SBP, urine protein and NO concentration were significantly improved with dose-dependent (all p < 0.05). In the cell experiment, the cell invasion and migration ability were significantly improved with Sal B supplement (both p < 0.05). However, with miRNA-155 transfection, the cell invasion and migration ability were suppressed with Sal B treatment (both p < 0.05). Conclusions Sal B improved preeclampsia via regulation of miRNA-155/CXCR4 in the in vitro and vivo study.

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