电针刺足三里穴对脓毒症大鼠心脏损害机制的研究
전침자족삼리혈대농독증대서심장손해궤제적연구
Effect of electro-acupuncture at Zusanli point on the injury of the heart function in sepsis rats
  • 万方数据
    中华实验外科杂志 중화실험외과잡지
    CHINESE JOURNAL OF EXPERIMENTAL SURGERY
    2013年 8期 1564-1567 ,共4页

    许涛%曹好好%许美霞%杨涛%李建国

    허도%조호호%허미하%양도%리건국

    脓毒血症%足三里%基质金属蛋白酶%胆碱能抗炎通路 膿毒血癥%足三裏%基質金屬蛋白酶%膽堿能抗炎通路
    농독혈증%족삼리%기질금속단백매%담감능항염통로
    Sepsis%Zusanli matrix metalloproteinases%Matrix metalloproteinase%Cholinergic anti-inflammatory pathway
    目的 探讨电针足三里穴对脓毒症大鼠心脏功能和结构的影响及机制.方法 将24只SD成年大鼠随机分为假手术组+电针非经非穴组(N +SEA),假手术+电针足三里组(N+EA),脓毒症+电针足三里组(CLP+ EA),脓毒症+电针非经非穴组(CLP+ SEA),共4组(n=6).采用盲肠结扎穿孔术(CLP)法制备大鼠脓毒症模型.N+EA组和CLP+ EA组电针足三里穴,N+SEA组和CLP+ SEA组电针非经非穴.6h后,摘除心脏固定于Langendofff灌流装置；置入左心导管,测定大鼠心脏左室舒张末压(LVEDP)、左心室收缩末期压力(LVSP),左室压最大上升速率(dp/dtmax)、心脏输出量(CO)和心率(HR).最后取心脏组织行免疫组织化学和实时定量聚合酶链反应(Real-time PCR)检测基质金属蛋白酶(MMP)-2、MMP-9及金属蛋白酶组织抑制因子(TIMP)-1、TIMP-2的表达.结果 CLP+ SEA组LVEDP[(5.2±0.9) mm Hg(1 mmHg=0.133 kPa)]、LVSP[(95.2 ±9.3)mm Hg],dp/dt max[(1804±122) mm Hg/s]、CO[(26.6±4.0)ml/min]和HR[(237±15) bpm],均较N+SEA组LVEDP[(9.9±1.6) mm Hg、LVSP[(127.8 ±8.7)mm Hg],dp/dt max[(2484 ±98) mm Hg/s]、CO[(43.10 ±5.30) ml/min]和HR[(310±12) bpm],N+ EA组LVEDP[(9.6±1.7) mmHg]、LVSP[(128.3±9.9)mm Hg],dp/dt max[(2536±107) mm Hg/s]、CO (45.9±5.7) ml/min和HR(312±15) bpm,明显降低(P＜0.01),而CLP+EA组LVEDP[(7.9±0.9) mm Hg]、LVSP[(112.0±11.9) mm Hg],dp/dt max[(2270±152) mm Hg/s]、CO[(35.6±5.1) ml/min]和HR[(280±24) bpm],较CLP+ SEA组明显改善(P＜0.01),在免疫组织化学检测中可见CLP+ SEA组MMP-2、MMP-9及TIMP-1、TIMP-2的表达明显增强,而CLP+ EA组MMP-2、MMP-9及T1MP-1、TIMP-2的表达则在一定程度上减弱.在mRNA水平上,CLP+ SEA组MMP-2(1.47±0.06)、MMP-9(1.59 ±0.04)、TIMP-2 (1.21±0.03)、TIMP-1(1.24±0.04)的mRNA表达明显增加(P＜0.01),而CLP+ EA组中MMP-2(1.30±0.09)、MMP-9(1.38±0.05)、TIMP-2(1.35±0.07)、TIMP-1(1.42±0.07)的表达较CLP+ SEA组均有不同程度的下降(P＜0.05).结论 电针刺足三里可减轻脓毒症大鼠心肌受损,改善血流动力学指标,其机制可能是电针刺足三里穴抑制了MMP-2和MMP-9的表达,改善两者与其特异性抑制剂表达的失衡,并同时激活了胆碱能抗炎通路.
    목적 탐토전침족삼리혈대농독증대서심장공능화결구적영향급궤제.방법 장24지SD성년대서수궤분위가수술조+전침비경비혈조(N +SEA),가수술+전침족삼리조(N+EA),농독증+전침족삼리조(CLP+ EA),농독증+전침비경비혈조(CLP+ SEA),공4조(n=6).채용맹장결찰천공술(CLP)법제비대서농독증모형.N+EA조화CLP+ EA조전침족삼리혈,N+SEA조화CLP+ SEA조전침비경비혈.6h후,적제심장고정우Langendofff관류장치；치입좌심도관,측정대서심장좌실서장말압(LVEDP)、좌심실수축말기압력(LVSP),좌실압최대상승속솔(dp/dtmax)、심장수출량(CO)화심솔(HR).최후취심장조직행면역조직화학화실시정량취합매련반응(Real-time PCR)검측기질금속단백매(MMP)-2、MMP-9급금속단백매조직억제인자(TIMP)-1、TIMP-2적표체.결과 CLP+ SEA조LVEDP[(5.2±0.9) mm Hg(1 mmHg=0.133 kPa)]、LVSP[(95.2 ±9.3)mm Hg],dp/dt max[(1804±122) mm Hg/s]、CO[(26.6±4.0)ml/min]화HR[(237±15) bpm],균교N+SEA조LVEDP[(9.9±1.6) mm Hg、LVSP[(127.8 ±8.7)mm Hg],dp/dt max[(2484 ±98) mm Hg/s]、CO[(43.10 ±5.30) ml/min]화HR[(310±12) bpm],N+ EA조LVEDP[(9.6±1.7) mmHg]、LVSP[(128.3±9.9)mm Hg],dp/dt max[(2536±107) mm Hg/s]、CO (45.9±5.7) ml/min화HR(312±15) bpm,명현강저(P＜0.01),이CLP+EA조LVEDP[(7.9±0.9) mm Hg]、LVSP[(112.0±11.9) mm Hg],dp/dt max[(2270±152) mm Hg/s]、CO[(35.6±5.1) ml/min]화HR[(280±24) bpm],교CLP+ SEA조명현개선(P＜0.01),재면역조직화학검측중가견CLP+ SEA조MMP-2、MMP-9급TIMP-1、TIMP-2적표체명현증강,이CLP+ EA조MMP-2、MMP-9급T1MP-1、TIMP-2적표체칙재일정정도상감약.재mRNA수평상,CLP+ SEA조MMP-2(1.47±0.06)、MMP-9(1.59 ±0.04)、TIMP-2 (1.21±0.03)、TIMP-1(1.24±0.04)적mRNA표체명현증가(P＜0.01),이CLP+ EA조중MMP-2(1.30±0.09)、MMP-9(1.38±0.05)、TIMP-2(1.35±0.07)、TIMP-1(1.42±0.07)적표체교CLP+ SEA조균유불동정도적하강(P＜0.05).결론 전침자족삼리가감경농독증대서심기수손,개선혈류동역학지표,기궤제가능시전침자족삼리혈억제료MMP-2화MMP-9적표체,개선량자여기특이성억제제표체적실형,병동시격활료담감능항염통로.
    Objective To discuss the effect of electro-acupuncturing at Zusanli point of the heart function and the structure of the rats with sepsis and the mechanism.Methods Twenty-four SD rats were randomly into four groups:N + SEA group,N + EA group,CLP + EA group,CLP + SEA group (n =6 each).The cecum ligation perforation technique (CLP) was used to prepare rat model of sepsis.In N + EA group and CLP + EA group,the rats were given electroacupuncture Zusanli point.In N + SEA group and CLP + SEA group the rats were given electroacupuncture at the point far from the Zusanli point.After 6 h the heart were quickly removed and fixed in Langendorff perfusion device.The left cardiac catheterization from pulmonary vein was done,and the left ventricular end-diastolic pressure (LVEDP),left ventricular end systolic pressure (LVSP),left ventricular pressure maximum rising rate (dp/dt max),cardiac output (CO)and heart rate (HR) were determined.The heart tissue was taken for detection of the expression of matrix metalloproteinase (MMP)-2,MMP-9 and tissue inhibitor of metalloproteinase (TIMP)-1,TIMP-2 by using immunohistochemical staining and real time quantitative polymerase chain reaction (Real-time PCR).Results In CLP +SEA group,LVEDP [(5.2 ±0.9) mm Hg (1 mm Hg =0.133 kPa)],LVSP [(95.2 ±9.3) mm Hg],dp/dt max [(1804 ±122) mm Hg/s],CO [(26.6 ±4.0) ml/min] and HR [(237 ± 15)/min] were decreased obviously as compared with N + EA group [LVEDP (9.9 ± 1.6) mm Hg,LVSP (127.8 ±8.7) mm Hg,dp/dt max (2484 ±98) mm Hg/s,CO (43.1 ±5.30) ml/min and HR (310 ±12)/min] and N + EA group [LVEDP (9.6 ± 1.7) mm Hg,LVSP (128.3 ± 9.9) mm Hg,dp/dt max (2536±107) mm Hg/s,CO (45.9 ±5.7) ml/min and HR (312 ± 15)/min] (P＜0.01 for all).Ascompared with CLP ±SEA group,LVEDP [(7.9 ±0.9) mm Hg],LVSP [(112.0 ± 11.9) mm Hg],dp/dt max [(2270 ± 152) mm Hg/s],CO [(35.6 ±5.1) ml/min],HR [(280 ±24)/min] in CLP +EA gourp were increased obviously (P ＜ 0.01).In CLP + SEA group,the expression of MMP-2,MMP-9,TIMP-1 and TIMP-2 was strengthened obviously,while that was weakened in CLP + SEA group.The mRNA expression of MMP-2 (1.47 ±0.06),MMP-9 (1.59 ±0.04),TIMP-2 (1.21 ±0.03) and TIMP-1 (1.24 ±0.04) was increased in CLP +SEA group,while that of MMP-2 (1.30 ±0.09),MMP-9 (1.38 ±0.05),TIMP-2 (1.35 ± 0.07) and TIMP-1 (1.42 ± 0.07) in CLP + EA group was reduced to varying degrees (P ＜0.05).Conclusion Electro-acupuncturing at Zusanli point can ease the injury of heart in rats with sepsis,improve the hemodynamics,which might be related to the fact that the electric acupuncture inhibits the expression of MMP-2 and MMP-9,improving the imbalance of them to their specific inhibitots,and at the same time activating the cholinergic anti-inflammatory pathway.
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