Alleviative Effects of Ciprofol on Hepatic Ischemia/Reperfusion Injury Through Inhibiting Macrophage Polarization

Previous studies have demonstrated the protective role of ciprofol against ischemia/reperfusion (I/R) injury, with the present investigation focusing on elucidating its effects on hepatic I/R injury.

A hepatic I/R injury animal model was established, and macrophages were polarized using lipopolysaccharide (LPS) induction. Hepatic tissue damage and apoptosis were assessed through hematoxylin-eosin and TUNEL staining. Liver function parameters, including aspartate aminotransferase (AST) and alanine aminotransferase (ALT), as well as pro-inflammatory cytokine levels, were quantified using commercial assay kits. Macrophage polarization was evaluated via quantitative real-time PCR, immunofluorescence, and immunoblotting, with flow cytometry additionally employed to assess cellular polarization. Pro-inflammatory cytokine concentrations were also measured.

In the I/R model mice, ciprofol, comparable to the positive control propofol, and the macrophage eliminator gadolinium chloride (GdCl₃) effectively attenuated inflammation and apoptosis, restored hepatic function, and inhibited macrophage polarization, as evidenced by reduced pro-inflammatory cytokine levels. In LPS-induced macrophages, ciprofol treatment decreased the proportion of CD86-positive cells and the expression of macrophage polarization markers, alongside a reduction in pro-inflammatory cytokine levels, mirroring the effects observed with propofol.

These findings suggest that ciprofol exerts hepatoprotective effects against I/R injury by modulating macrophage polarization.