实用临床医药杂志2025，Vol.29Issue(11)：42-48,7.DOI:10.7619/jcmp.20250611
人参总皂苷调控SLC7A11/GPX4介导的铁死亡减轻脓毒症模型大鼠心肌损伤的机制研究
Mechanism of total ginsenosides in alleviating myocardial injury in septic rat models by regulating SLC7A11/GPX4-mediated ferroptosis
摘要
Abstract
Objective To investigate the mechanism of total ginsenosides(TG)in alleviating myocardial injury in septic rat models by regulating solute carrier family 7 member 11/glutathione per-oxidase 4(SLC7 A1 1/GPX4)-mediated ferroptosis.Methods Ninety SPF-grade male rats were ran-domly divided into five groups:Sham group(sham operation),septic cardiomyopathy(SCM)group,TG40 group(SCM model rats gavaged with 40 mg/kg TG),TG160 group(SCM model rats gavaged with 160 mg/kg TG),and TG160+RSL3 group(SCM model rats gavaged with 160 mg/kg TG and intraperitoneally injected with 10 mg/kg ferroptosis inducer RSL3).The SCM model was established using the cecal ligation and puncture method.Cardiac function was assessed in each group.Hematox-ylin-eosin(HE)staining was performed to observe pathological changes in myocardial tissue.Levels of tumor necrosis factor(TNF)-α,interleukin(IL)-1 β,IL-6,creatine kinase-MB(CK-MB),myo-globin(Mb),and cardiac troponin I(cTnI)were measured by enzyme-linked immunosorbent assay.Protein expression levels of NADPH oxidase(NOX)1,NOX2,NOX4,SLC7A11,and GPX4 were detected by western blotting.Levels of Fe2+and total iron in myocardial tissue were also determined.Results Compared with the Sham group,the SCM group exhibited decreased left ventricular ejec-tion fraction(LVEF),left ventricular fractional shortening(LVFS),and protein expression of SLC7A11 and GPX4,along with increased levels of CK-MB,Mb,cTnI,TNF-α,IL-1β,IL-6,Fe2+,total iron,and protein expression of NOX1,NOX2,and NOX4(P＜0.05).Compared with the SCM group,the TG40 and TG160 groups showed dose-dependent increases in LVEF,LVFS,and SLC7A11/GPX4 expression,as well as reductions in CK-MB,Mb,cTnI,TNF-α,IL-1 β,IL-6,Fe,total iron,and NOX1/NOX2/NOX4 expression(P＜0.05).In contrast,the TG160+RSL3 group displayed lower LVEF,LVFS,and SLC7A11/GPX4 expression,and higher levels of the aforementioned biomarkers compared with the TG160 group(P＜0.05).Conclusion TG sig-nificantly suppresses sepsis-induced myocardial inflammation and oxidative stress,improves cardiac function,and mitigates myocardial injury,likely by inhibiting ferroptosis via activation of the SLC7A11/GPX4 signaling pathway.关键词
人参总皂苷/溶质载体家族7成员11/谷胱甘肽过氧化物酶4/铁死亡/脓毒症心肌病/有丝分裂氧化酶/肿瘤坏死因子/心肌肌钙蛋白Key words
total ginsenosides/solute carrier family 7 member 11/glutathione peroxidase 4/ferroptosis/septic cardiomyopathy/NADPH oxidase/tumor necrosis factor/cardiac troponin分类
医药卫生引用本文复制引用
张科凤,刘一诚,罗琳,张婷..人参总皂苷调控SLC7A11/GPX4介导的铁死亡减轻脓毒症模型大鼠心肌损伤的机制研究[J].实用临床医药杂志,2025,29(11):42-48,7.基金项目
2021年四川省医学(青年创新)科研项目(S211039) （青年创新）
