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

## TL;DR

Ciprofol protects the liver from injury during blood flow restoration by reducing inflammation and preventing immune cell activation.

## Contribution

This study reveals that ciprofol inhibits macrophage polarization to protect the liver from ischemia/reperfusion injury.

## Key findings

- Ciprofol reduced liver inflammation and apoptosis in a mouse model of I/R injury.
- Ciprofol suppressed macrophage polarization and pro-inflammatory cytokine levels.
- Ciprofol's effects were comparable to propofol and macrophage elimination with GdCl3.

## Abstract

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.

This study investigates the protective effects of ciprofol on hepatic ischemia/reperfusion (I/R) injury, demonstrating that it reduces inflammation and apoptosis in liver tissue. Using a mouse model, ciprofol treatment was shown to suppress macrophage polarization and decrease pro‐inflammatory cytokine levels, similar to the effects observed with the positive control propofol. These findings suggest that ciprofol may offer a protective mechanism against liver I/R injury by inhibiting macrophage activation.