■脓毒症是一种全身性炎症性疾病,和BrevilinA(BA)具有强大的抗炎作用。然而,BA对脓毒性心肌病是否有类似的作用尚不清楚.本研究旨在探讨BA在脓毒性心肌病中的作用及机制。
■首先,在体外和体内建立了化脓性心肌病模型。心脏损伤标志物的表达,通过实时聚合酶链反应和蛋白质印迹法检测NOD样受体家族pyrin结构域3(NLRP3)炎症因子及其上游调节剂NF-κB。使用超声心动图测量心功能,使用甲基噻唑基四唑盐测定法检测细胞活力。为了进一步研究BA对脓毒性心肌病的影响,使用不同浓度的BA。实验分为对照组,LPS诱导组,LPS+2.5、5.0、10.0μMBA处理组的体外模型,还有Sham,CLP,CLP+10、20、30mg/kgBA医治组的年夜鼠体内模子。最后,心脏损伤,NLRP3炎症,并评估各组的心功能。
■在体外和体内脓毒症心肌病模型中,心脏炎症和损伤基因的mRNA和蛋白表达均显着增加。当不同浓度的BA用于体内和体外脓毒症心肌病时,上述心肌炎症和损伤因素均得到不同程度的抑制,细胞活力增加,心功能改善,老鼠的存活率也提高了。
■BA通过抑制NF-κB/NLRP3炎症激活改善脓毒症心肌病。
UNASSIGNED: Sepsis is a systemic inflammatory disease, and Brevilin A (
BA) has a powerful anti-inflammatory effect. However, whether
BA has a similar effect on septic cardiomyopathy remains unclear. This study aimed to investigate the effect and mechanism of
BA in septic cardiomyopathy.
UNASSIGNED: First, a model of septic cardiomyopathy was constructed in vitro and in vivo. The expression of the cardiac injury markers, NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammation factors and its upstream modulator NF-κB was detected by real-time polymerase chain reaction and western blotting. Cardiac function was measured using echocardiography, cell viability was detected using the methyl thiazolyl tetrazolium assay. To further investigate the effects of
BA on septic cardiomyopathy, different concentrations of
BA were used. The experiment was divided into control group, LPS induced- group, LPS+2.5, 5.0, 10.0 μM
BA treatment group of the vitro model, and the Sham, CLP, CLP+10, 20, 30 mg/kg BA treatment groups of the rat vivo model. Lastly, cardiac injury, NLRP3 inflammation, and cardiac function were assessed in each group.
UNASSIGNED: The mRNA and protein expression of cardiac inflammation and injury genes were significantly increased in the in vitro and in vivo sepsis cardiomyopathy models. When different concentrations of BA were used in sepsis cardiomyopathy in vivo and in vitro, the above-mentioned myocardial inflammation and injury factors were suppressed to varying degrees, cell viability increased, cardiac function improved, and the survival rate of rats also increased.
UNASSIGNED: BA ameliorated sepsis cardiomyopathy by inhibiting NF-κB/NLRP3 inflammation activation.