Etomidate is a commonly used short-acting intravenous anesthetic and has become an important option for anesthesia induction in myocardial injury patients. However, the potential molecular mechanisms underlying the cardioprotective effect of etomidate remain to be revealed. Human cardiomyocytes (AC16) were exposed PM2.5 to induce cell injury. Cell viability and apoptosis were analyzed by CCK8 assay and flow cytometry. LDH release was determined to assess cytotoxicity. The levels of MDA, GSH, Fe 2+ and ROS were detected to analyze cell ferroptosis. The expression levels of heat shock cognate B (HSCB) and ferroptosis-related markers were examined by qRT-PCR or western blot. Two datasets (GSE95506 and GSE212044) were obtained from the GEO database to analyze differentially expressed genes. Etomidate promoted viability and inhibited PM2.5-induced cytotoxicity, apoptosis and ferroptosis in AC16 cells in a dose-dependent manner. A total of 3 differentially expressed genes (NSMF, HSCB and SUB1) were screened by GEO database, among which HSCB was lowly expressed in PM2.5-induced AC16 cells and was overexpressed after etomidate treatment. Further analysis indicated that HSCB overexpression alleviated PM2.5-induced cytotoxicity, apoptosis and ferroptosis, and its knockdown reversed the protective effect of etomidate on myocardial injury. Etomidate relieved PM2.5-induced cardiomyocyte injury by upregulating HSCB expression, providing a new insight into the cardioprotective effect of etomidate. • Etomidate inhibits PM2.5-induced cytotoxicity, apoptosis and ferroptosis. • HSCB is upregulated by etomidate in PM2.5-induced cardiomyocytes. • Etomidate enhances HSCB expression to relieve PM2.5-induced cardiomyocyte injury.
Liu et al. (Sun,) studied this question.