Propofol Ameliorates Spinal Cord Injury Process by Mediating miR-672-3p/TNIP2 Axis.

Abstract

Propofol has been found to have a protective effect against spinal cord injury (SCI). However, the underlying molecular mechanism of propofol regulating SCI process remains unclear. In this study, lipopolysaccharide (LPS)-induced PC12 cells were used to build SCI cell models. Cell viability and apoptosis were determined by cell counting kit 8 assay, flow cytometry, and caspase-3 activity detection. The protein levels of apoptosis-related markers and TNFAIP3 interacting protein 2 (TNIP2) were assessed using western blot analysis, and the levels of inflammatory factors were detected using ELISA. Cell oxidative stress was evaluated by measuring malondialdehyde (MDA) and reactive oxygen species (ROS) levels. The expression of microRNA (miR)-672-3p was examined by quantitative real-time PCR. SCI rat models were constructed to assess the effect of propofol in vivo. We found that propofol treatment promoted viability, while inhibited apoptosis, inflammation and oxidative stress of LPS-induced PC12 cells. Propofol decreased miR-672-3p expression, and miR-672-3p overexpression eliminated the inhibiting effect of propofol on LPS-induced PC12 cell injury. Besides, miR-672-3p targeted TNIP2, and TNIP2 knockdown reversed the protective effect of miR-672-3p inhibitor or propofol against LPS-induced PC12 cell injury. In vivo experiments, propofol treatment enhanced the motor function recovery and inhibited apoptosis of SCI rat models. In conclusion, propofol increased TNIP2 level by reducing miR-672-3p expression, thereby alleviating LPS-induced PC12 cell injury and improving the motor function of SCI rat models.