摘要
Abstract
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(CK-MB),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.关键词
瑞马唑仑/脓毒症/心肌损伤/心肌/炎症/凋亡Key words
remimazolam/sepsis/myocardial injury/cardiac muscle/inflammation/apoptosis分类
基础医学
