中国心血管杂志
中國心血管雜誌
중국심혈관잡지
CHINESE JOURNAL OF CARDIOVASOLOGY
2013年
3期
210-213
,共4页
心肌营养素-1%糖蛋白130%替米沙坦%心室重构%大鼠
心肌營養素-1%糖蛋白130%替米沙坦%心室重構%大鼠
심기영양소-1%당단백130%체미사탄%심실중구%대서
CT-1 mRNA%GP130%Telmisartan%Ventricular remodeling%Rats
目的 观察心肌营养素-1(CT-1)和糖蛋白130(GP130)在压力超负荷性大鼠心肌中的表达变化与心室重构的关系,以及替米沙坦对心室重构及CT-1和GP130表达的影响.方法 20只雄性SD大鼠行腹主动脉缩窄术后2周制成压力负荷性心肌肥厚模型,随机分为左心室肥厚组(LVH)(10只)和替米沙坦组(Tel)(10只),另设8只作为假手术组(Sham).替米沙坦组灌胃给药(3 mg·kg-1·d-1),连续4周.测定血流动力学指标和心室质量指数,放射免疫法测定心肌血管紧张素Ⅱ(AngⅡ)含量,原位杂交法检测心肌的CT-1 mRNA表达水平；免疫组化法检测心肌中GP130蛋白水平表达.结果 与假手术组比较,肥厚组SBP、DBP和MBP显著升高(P=0.022,0.011,0.013),LVMI和RVMI亦明显升高(P =0.010,0.017)；心肌组织AngⅡ含量、CT-1 mRNA和GP130蛋白表达水平明显增加(P＜0.01,P=0.032,0.021).相关分析表明,心肌组织中CT-1 mRNA和GP130的蛋白表达与AngⅡ及LVMI呈显著正相关(均为P＜0.05).替米沙坦改善血流动力学指标相比较肥厚组显著降低(P =0.041,0.021,0.019),降低LVMI和RVMI(P=0.038,0.042),血浆AngⅡ含量显著增加,心肌AngⅡ含量显著降低(均为P＜0.01),CT-1 mRNA和GP130蛋白表达明显下降(P=0.029,0.018).结论 压力超负荷性大鼠心肌中CT-1 mRNA及其受体GP130蛋白的过度表达与心室重构的发生密切相关；替米沙坦逆转心室重构的机制可能与抑制CT-1及受体GP130蛋白的过度表达相关.
目的 觀察心肌營養素-1(CT-1)和糖蛋白130(GP130)在壓力超負荷性大鼠心肌中的錶達變化與心室重構的關繫,以及替米沙坦對心室重構及CT-1和GP130錶達的影響.方法 20隻雄性SD大鼠行腹主動脈縮窄術後2週製成壓力負荷性心肌肥厚模型,隨機分為左心室肥厚組(LVH)(10隻)和替米沙坦組(Tel)(10隻),另設8隻作為假手術組(Sham).替米沙坦組灌胃給藥(3 mg·kg-1·d-1),連續4週.測定血流動力學指標和心室質量指數,放射免疫法測定心肌血管緊張素Ⅱ(AngⅡ)含量,原位雜交法檢測心肌的CT-1 mRNA錶達水平；免疫組化法檢測心肌中GP130蛋白水平錶達.結果 與假手術組比較,肥厚組SBP、DBP和MBP顯著升高(P=0.022,0.011,0.013),LVMI和RVMI亦明顯升高(P =0.010,0.017)；心肌組織AngⅡ含量、CT-1 mRNA和GP130蛋白錶達水平明顯增加(P＜0.01,P=0.032,0.021).相關分析錶明,心肌組織中CT-1 mRNA和GP130的蛋白錶達與AngⅡ及LVMI呈顯著正相關(均為P＜0.05).替米沙坦改善血流動力學指標相比較肥厚組顯著降低(P =0.041,0.021,0.019),降低LVMI和RVMI(P=0.038,0.042),血漿AngⅡ含量顯著增加,心肌AngⅡ含量顯著降低(均為P＜0.01),CT-1 mRNA和GP130蛋白錶達明顯下降(P=0.029,0.018).結論 壓力超負荷性大鼠心肌中CT-1 mRNA及其受體GP130蛋白的過度錶達與心室重構的髮生密切相關；替米沙坦逆轉心室重構的機製可能與抑製CT-1及受體GP130蛋白的過度錶達相關.
목적 관찰심기영양소-1(CT-1)화당단백130(GP130)재압력초부하성대서심기중적표체변화여심실중구적관계,이급체미사탄대심실중구급CT-1화GP130표체적영향.방법 20지웅성SD대서행복주동맥축착술후2주제성압력부하성심기비후모형,수궤분위좌심실비후조(LVH)(10지)화체미사탄조(Tel)(10지),령설8지작위가수술조(Sham).체미사탄조관위급약(3 mg·kg-1·d-1),련속4주.측정혈류동역학지표화심실질량지수,방사면역법측정심기혈관긴장소Ⅱ(AngⅡ)함량,원위잡교법검측심기적CT-1 mRNA표체수평；면역조화법검측심기중GP130단백수평표체.결과 여가수술조비교,비후조SBP、DBP화MBP현저승고(P=0.022,0.011,0.013),LVMI화RVMI역명현승고(P =0.010,0.017)；심기조직AngⅡ함량、CT-1 mRNA화GP130단백표체수평명현증가(P＜0.01,P=0.032,0.021).상관분석표명,심기조직중CT-1 mRNA화GP130적단백표체여AngⅡ급LVMI정현저정상관(균위P＜0.05).체미사탄개선혈류동역학지표상비교비후조현저강저(P =0.041,0.021,0.019),강저LVMI화RVMI(P=0.038,0.042),혈장AngⅡ함량현저증가,심기AngⅡ함량현저강저(균위P＜0.01),CT-1 mRNA화GP130단백표체명현하강(P=0.029,0.018).결론 압력초부하성대서심기중CT-1 mRNA급기수체GP130단백적과도표체여심실중구적발생밀절상관；체미사탄역전심실중구적궤제가능여억제CT-1급수체GP130단백적과도표체상관.
