Conclusions
The current study verified the anti-PE function of Pue: the compound suppressed inflammatory response associated with PE, and improved trophoblast motility. The effects depended on the inhibition of miR-181b-5p that inhibited the expression of RBAK.
Results
The induction of PE increased blood pressure and 24-h proteinuria, and induced TNF-α, IL-1β, and IL-6 levels, which was reversed by Pue. In in vitro assays, TNF-α suppressed viability, induced apoptosis and inflammatory response, and inhibited migration in trophoblasts, which was attenuated by Pue. At molecular level, the expression level of miR-181b-5p was both induced in vivo and in vitro with the development of PE symptoms, contributing to the inhibited expression of RBAK. The induced expression of miR-181b-5p under Pue treatment showed that the reinduction of miR-181b-5p counteracted the effects of Pue, indicating the key role of the miR in the protective effects of Pue against PE. Conclusions: The current study verified the anti-PE function of Pue: the compound suppressed inflammatory response associated with PE, and improved trophoblast motility. The effects depended on the inhibition of miR-181b-5p that inhibited the expression of RBAK.