Propofol Protects Cardiac Myocytes from H2O2-induced Cell Injury via Regulating ROS Accumulation and Mitochondrial Function from Oxidative Stress via Regulating ROS and Mitochondria

Abstract

Oxidative stress is one of the main mechanisms of myocardial ischaemia-reperfusion (I/R)-induced injury, which is one of the main cause of cardiomyocyte death and precipitates life-threatening heart failure. Propofol (2,6-diisopropylphenyl, PR) plays critical roles, including in I/R-induced oxidative stress; however, its protective effects on I/R-induced oxidative stress are still largely unknown. Considering that oxidative stress strongly affects mitochondrial function, we hypothesized that propofol may regulate I/R-induced H9C2 injury by modifying mitochondrial function. In a H2O2-induced cell model, propofol treatment reversed the H2O2-induced blockade of the cell cycle at the G1 phase and promotion of apoptosis. Two-hour pretreatment promoted proliferation and inhibited apoptosis, indicating that propofol pretreatment may, decrease H2O2-induced ROS accumulation. Propofol decreased oxidative stress-induced haem oxygenase-1 (HO-1) expression, and ROS scavenging mediated by treatment with NAC also decreased HO-1 expression. Propofol decreased ROS accumulation after H2O2 treatment, which was similar to the effects of the ROS scavenger NAC. Further results also showed that propofol enhanced the maintenance of mitochondrial function. However, without affecting the mitochondrial DNA content, propofol decreased mitochondrial ATP production and transcriptional activity, indicating that propofol may temporarily block mitochondrial function to prevent oxidative stress. These results suggest that propofol protects cardiomyocytes by regulating mitochondrial function.