Propofol Attenuates Inflammatory Response in LPS-Activated Microglia by Regulating the miR-155/SOCS1 Pathway.

Propofol is a widely used intravenous anesthetic agent with potential neuroprotective effect in diverse models of neuronal injury, including ischemic stroke and traumatic brain injury. However, few studies have been carried out to determine the effects and molecular mechanisms of propofol in classic microglial activation (M1 activation) related to neuronal injury. This study explored the anti-inflammatory effects of propofol in LPS-activated BV2 microglia. Propofol potently decreased the pro-inflammatory mediators, such as nitric oxide, TNF-α, and IL-6, at both the transcriptional and translational levels. Furthermore, propofol suppressed the expression of miR-155 in LPS-activated cells. Knockdown of miR-155 attenuated the anti-inflammatory effect of propofol in cells after LPS exposure. miR-155 was also confirmed as a negative regulator of SOCS1 expression. The inhibitory effect of propofol on LPS-induced inflammation involved the upregulation of SOCS1. Overall, these results suggest that propofol can suppress the neuroinflammatory response of microglia to LPS through the regulation of the miR-155/SOCS1 pathway.