Propofol maintains Th17/Treg cell balance and reduces inflammation in rats with traumatic brain injury via the miR-145-3p/NFATc2/NF-[kappa]B axis

Propofol is a commonly used intravenous anesthetic. The aim of the study was to examine the mechanism of propofol in traumatic brain injury (TBI) by regulating interleukin (IL)-17 activity and maintaining the Th17/Treg balance. A rat model with moderate TBI was established using the weight-drop method. Rats with TBI were regularly injected with propofol and their brain injuries were monitored. The peripheral blood of rats was collected to measure the Th17/Treg ratio. MicroRNA (miR)-145-3p expression was detected in the brain tissues of rats and antagomiR-145-3p was injected into the lateral ventricles of their brains to verify the effect of miR-145-3p on brain injury. The downstream target of miR-145-3p was predicted. The targeting relationship between miR-145-3p and nuclear factor of activated T cells c2 (NFATc2) was confirmed. NFATC2 expression and phosphorylation of NF-[kappa]B pathway-related proteins were measured. Propofol alleviated brain injury in rats with TBI and maintained the Th17/Treg balance. Propofol upregulated miR-145-3p expression in rat brains, while the inhibition of miR-145-3p reversed the effect of propofol on brain injury. A binding relationship was observed between miR-145-3p and NFATc2. Furthermore, propofol decreased the phosphorylation of p65 and I[kappa]B[alpha], and inhibited activation of the NF-[kappa]B pathway in the brains of rats with TBI. In conclusion, propofol maintained Th17/Treg balance and reduced inflammation in the rats with TBI via the miR-145-3p/NFATc2/NF-[kappa]B axis. Key words: propofol, traumatic brain injury, microRNA-145-3p, nuclear factor of activated T cells c2, Th17/Treg, NF-[kappa]B, inflammation