Propofol maintains Th17/Treg cell balance and reduces inflammation in rats with traumatic brain injury via the miR‑145‑3p/NFATc2/NF‑κB 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‑κB 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 IκBα, and inhibited activation of the NF‑κB 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‑κB axis.