Objective: To investigate the effects of remimazolam on sepsis-induced myocardial injury in rats by
regulating the NOD-like receptor thermal protein domain associated protein 3 (NLRP3)/interleukin (IL)-1β signaling
pathway. Methods: Mice were randomly divided into seven groups: cecal ligation and puncture (CLP) group, control
group, low-dose remimazolam group, high-dose remimazolam group, ampicillin group, and high-dose remimazolam+
NLRP3 activator (DDC) group. Except for the control group, sepsis models were induced in the other groups via
CLP surgery. After successful modeling, drug administration was performed once a day for two consecutive days.
The changes in left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) in mice
were detected. ELISA was performed to detected the levels of lactate dehydrogenase (LDH), creatine kinase (CKMB),
and cardiac troponin I (cTnI) in serum, and the levels of IL-6, IL-18, and tumor necrosis factor alpha (TNF-α)
in myocardial tissue. H-E staining was utilized to assess myocardial pathology. TUNEL staining was employed to
measure cell apoptosis in myocardial tissue. Western blotting was conducted to measure p53, Bcl-2 associated X
protein (Bax), NLRP3, and IL-1β protein in myocardial tissue. Results: Remimazolam can improve myocardial
injury in mice, as evidenced by increased LVEF and LVEF and decreased levels of LDH, CK-MB, cTNI in serum,
along with the decreased levels of IL-6, IL-18, TNF-α in myocardial tissue. It also decreased the apoptosis rate and
the levels of p53, Bax, NLRP3, and IL-1β protein. DDC reversed the inhibitory effect of high-dose remimazolam
on inflammation and cell apoptosis in mice with sepsis-induced myocardial injury. Conclusion: Remimazolam may
alleviate sepsis-induced myocardial injury by inhibiting the NLRP3/IL-1β signaling pathway, thereby reducing
inflammation and apoptosis in mice.