Abstract: Objective To study the effect of midazolam on lipopolysaccharide ( LPS) -induced H9c2 cardiomyocyte damage and its molecular biological mechanism. Methods H9c2 cell viability was compared under stimulation with midazolam and LPS at different concentrations and time points to determine the optimal administration conditions for midazolam. H9c2 cardiomyocytes were divided into control group, midazolam group, LPS group and LPS + midazolam group. Cell apoptosis rate, mitochondrial membrane potential changes, oxidative stress indicators, levels of inflammatory factors and expression levels of NOD-like receptor protein3 (NLRP3) / caspase-1 pathway-related proteins were compared among the groups. The effect of midazolam was validated with NLRP3 activator nigericin. Results Midazolam can reduce the apoptosis rate of LPS-induced H9c2 cardiomyocytes, alleviate the oxidative stress response and inflammatory response, and enhance the expression levels of NLRP3 / caspase-1 pathway-related proteins. Conclusion Midazolam has a protective effect on LPS-induced H9c2 cardiomyocyte damage. Its mechanism may be related to the inhibition of NLRP3 / caspase-1 signaling pathway

Key words: midazolam, lipopolysaccharide, cardiomyocytes, NLRP3 / caspase-1 pathway, nigericin