Sufentanil alleviates pre-eclampsia via silencing microRNA-24-3p to target 11β-Hydroxysteroid dehydrogenase type 2

Pre-eclampsia (PE) is a prevalent pregnancy disease characterized by insufficient trophoblast cell migration (HTR8/SVneo). Consequently, accelerating trophoblast cell proliferation might ameliorate PE. This study assessed the effects and molecular mechanisms of Sufentanil (SUF) on HTR8/SVneo cells proliferation. HTR8/SVneo cells and PE clinical samples were used. Peripheral blood was collected from PE patients' samples, and microRNA (miR)-24-3p and 11 beta-hydroxysteroid dehydrogenase type 2 (HSD11B2) was analyzed in the blood and cells. HTR8/SVneo cells were treated with varying SUF concentrations or transfected with miR-24-3p mimics/inhibitors, or HSD1162 elevation vector. CCK-8, colony formation, transwell, and flow cytometry assays were then carried out. Association of miR-24 - 3p with HSD1162 was investigated. PE animal model was constructed using Wistar rats to verify SUF's role on PE in vivo. According to the results, SUF boosted HTR8/SVneo cell proliferation, and inhibited miR-24-3p to accelerate HSD11B2. MiR-24-3p was increased in PE, while HSD1162 was inhibited, and miR-24-3p targeted HSD11B2. HSD1162 reversed miR-24-3p's repression on HTR/SVneo cell advancement. SUF restrained PE's progression in vivo and in vitro via mediating the miR-24-3p/HSD11B2 axis. In conclusion, SUF enhances HSD1162 via repressing miR-24-3p, thereby suppressing PE's progression. The study provides an insight into the possibility of using SUF as a novel therapeutic target for PE, which acts via combining with miR-24-3p.

Automated summary

This study found that Sufentanil (SUF) enhances HTR8/SVneo cell proliferation by inhibiting miR-24-3p and promoting HSD11B2 expression. In patients with pre-eclampsia, miR-24-3p is increased while HSD1162 is inhibited, and miR-24-3p targets HSD11B2. Additionally, SUF restrains the progression of pre-eclampsia in vivo and in vitro by mediating the miR-24-3p/HSD11B2 axis.