陕西医学杂志
陝西醫學雜誌
협서의학잡지
SHAANXI MEDICAL JOURNAL
2015年
6期
643-645
,共3页
脓毒症%心脏损伤%钠氢交换蛋白1
膿毒癥%心髒損傷%鈉氫交換蛋白1
농독증%심장손상%납경교환단백1
Sepsis%Heartinjuries%Na+/H+exchanger1
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(CK‐MB)、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:N H E1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。
目的:觀察鈉氫交換蛋白1(NHE1)抑製劑對膿毒癥大鼠心髒損傷的保護作用,併探討其可能的機製。方法:常規方法建立大鼠膿毒癥模型誘導心髒損傷。將SD大鼠隨機分為對照組、膿毒癥組和膿毒癥治療組,膿毒癥治療組大鼠註射鈉氫交換蛋白1抑製劑卡立泊來德,于傷後12h檢測左心室射血分數(LVEF)、乳痠脫氫酶(LDH)、肌痠激酶(CK)、肌痠激酶同工酶(CK‐MB)、腫瘤壞死因子α(TNF‐α)、白細胞介素6(IL‐6)、髓過氧化物酶(MPO)、超氧化物歧化酶(SOD)、過氧化氫酶(CAT)、穀胱甘肽過氧化物酶(GPx)和丙二醛(MDA)水平。結果:膿毒癥組大鼠心髒損傷高于對照組,錶現為LVEF值的降低和LDH、CK、CK‐MB值的升高;膿毒癥治療組大鼠較膿毒癥組大鼠心髒損傷顯著減輕,錶現為 LVEF值的升高、LDH、CK 和CK‐MB值的降低。膿毒癥組大鼠TNF‐α、IL‐6、MPO、MDA水平高于對照組,差異有統計學意義;SOD、CAT 和GPx水平低于對照組,差異有統計學意義;治療組大鼠上述指標顯著改善。結論:N H E1抑製顯著減輕膿毒癥誘導的心髒損傷,其部分機製可能是抑製瞭炎癥反應和氧化應激。
목적:관찰납경교환단백1(NHE1)억제제대농독증대서심장손상적보호작용,병탐토기가능적궤제。방법:상규방법건립대서농독증모형유도심장손상。장SD대서수궤분위대조조、농독증조화농독증치료조,농독증치료조대서주사납경교환단백1억제제잡립박래덕,우상후12h검측좌심실사혈분수(LVEF)、유산탈경매(LDH)、기산격매(CK)、기산격매동공매(CK‐MB)、종류배사인자α(TNF‐α)、백세포개소6(IL‐6)、수과양화물매(MPO)、초양화물기화매(SOD)、과양화경매(CAT)、곡광감태과양화물매(GPx)화병이철(MDA)수평。결과:농독증조대서심장손상고우대조조,표현위LVEF치적강저화LDH、CK、CK‐MB치적승고;농독증치료조대서교농독증조대서심장손상현저감경,표현위 LVEF치적승고、LDH、CK 화CK‐MB치적강저。농독증조대서TNF‐α、IL‐6、MPO、MDA수평고우대조조,차이유통계학의의;SOD、CAT 화GPx수평저우대조조,차이유통계학의의;치료조대서상술지표현저개선。결론:N H E1억제현저감경농독증유도적심장손상,기부분궤제가능시억제료염증반응화양화응격。
Objective:This study was designed to investigate the cardioprotective role of Na+ /H+ ex‐changer 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 .