Fibrinogen-like protein 2 aggravates myocardial ischemia/reperfusion injury in mice following sevoflurane anesthetic through ROS production by PPAR

This study aims to investigate the mechanism and effects of Fibrinogen-like protein 2 (FGL2) in myocardial ischemia/reperfusion injury in mice following sevoflurane anesthetic. Mice of SAP group were placed in box with oxygen and anesthetic gas (60 mg/kg, pentobarbital), 2.5% Sevoflurane was pumped into the box for 1 h. H9C2 cells were treated by 3% sevoflurane for 6 h and a mixture of 95% O2 + 5% CO2 for 24 h. Fg12 mRNA expression was up-regulated in mice of I/R injury following sevoflurane. Fgl2 protein reduced HR, LVDP, dp/dtmax (+) and dp/dtmax (-), increased LVEDP levels, myocardial infarct size and AI in mice of I/R injury following sevoflurane. Fgl2 suppressed PPAR signaling pathway, and promoted ROS production in vivo or vitro model. The activation of PPAR signaling pathway reduced the function of Fgl2 in vivo and vitro model. Fgl2 might serve as a therapeutic target in the treatment of I/R injury following sevoflurane. We hope that our findings will pave a way for future therapies against I/R injury following sevoflurane.