摘要
目的:观察钠氢交换蛋白1(NHE1)抑制剂对脓毒症大鼠心脏损伤的保护作用,并探讨其可能的机制。方法:常规方法建立大鼠脓毒症模型诱导心脏损伤。将SD大鼠随机分为对照组、脓毒症组和脓毒症治疗组,脓毒症治疗组大鼠注射钠氢交换蛋白1抑制剂卡立泊来德,于伤后12h检测左心室射血分数(LVEF)、乳酸脱氢酶(LDH)、肌酸激酶(CK)、肌酸激酶同工酶(CKMB)、肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、髓过氧化物酶(MPO)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)和丙二醛(MDA)水平。结果:脓毒症组大鼠心脏损伤高于对照组,表现为LVEF值的降低和LDH、CK、CK-MB值的升高;脓毒症治疗组大鼠较脓毒症组大鼠心脏损伤显著减轻,表现为LVEF值的升高、LDH、CK和CK-MB值的降低。脓毒症组大鼠TNF-α、IL-6、MPO、MDA水平高于对照组,差异有统计学意义;SOD、CAT和GPx水平低于对照组,差异有统计学意义;治疗组大鼠上述指标显著改善。结论:NHE1抑制显著减轻脓毒症诱导的心脏损伤,其部分机制可能是抑制了炎症反应和氧化应激。
Objective：This study was designed to investigate the cardioprotective role of Na＋ /H＋ exchanger 1 （NHE1） inhibition after sepsis ,and explore the potential mechanisms .Methods ：A common sepsis model was used to induce cardiac injury in rats .All rats were randomly divided into 3 groups：the control group ,the sepsis group and the treatment group .Changes in left ventricular ejection fraction （LVEF） ,the lactate dehydrogenase （LDH） ,creatine kinase （CK） ,MB isoenzyme of creatine kinase （CK‐MB） ,tumor necrosis factor （TNF‐α） ,inter‐leukin （IL‐6） ,myeloperoxidase （MPO） activity ,superoxidase dismutase （SOD） ,catalase （CAT） ,glutathione per‐oxidase （GPx） and malondialdehyde （MDA） were examined .Results：Sepsis resulted in significant cardiac injury ,as manifested by lowered LVEF ,increased serum LDH ,CK and CK‐MB ,compared with the control group .NHE1 in‐hibition markedly alleviated cardiac injury .In addition ,sepsis caused increased level of TNF‐α、IL‐6、MPO and MDA ,and decreased of SOD、CAT and GPx ,which were improved by NHE1 inhibition in treatment group .Conclu‐sion：NHE1 inhibition alleviates sepsis‐induced cardiac injury ,possibly by inhibiting sepsis‐induced oxidative stress and inflammation response .
出处
《陕西医学杂志》
CAS
2015年第6期643-645,共3页
Shaanxi Medical Journal
基金
国家自然科学基金资助项目(81201463)
