The dual effects of propofol down-regulating PD-L1 expression and inhibiting autophagy to reduce cerebral ischemia reperfusion injury.

Propofol, an anesthetic, has shown neuroprotective effects in animal and cellular models of cerebral ischemia-reperfusion (I/R) injury, likely by suppressing I/R-induced excessive autophagy. PD-L1 and immune escape are implicated in experimental stroke outcomes, but their mechanisms remain unclear. Here, we demonstrate that oxygen-glucose deprivation/reoxygenation (OGD/R) in astrocytes upregulates PD-L1 expression and autophagy, effects that are attenuated by propofol treatment via the NF-κB pathway. In vivo, propofol protects mice from I/R injury by downregulating PD-L1, inflammatory factors, and autophagy. Clinically, craniotomy patients receiving propofol exhibited higher CD3+ and CD4+ T lymphocyte percentages and lower PD-L1 and inflammatory factor levels. Our findings elucidate propofol's dual role in downregulating PD-L1 and inhibiting autophagy in cerebral I/R injury, suggesting its potential as a novel therapeutic strategy to mitigate inflammation and immune dysregulation.