中文摘要：

目的：观察苓桂术甘汤对急性心肌梗死（acute myocardial infarction,AMI）后心室重构模型大鼠心肌组织核因子-κB（nuclear factor-κB,NF-κB）及NF-κB mRNA表达,血清NF-κB含量的影响,探讨苓桂术甘汤干预AMI后心室重构（ventricular remodeling,VR）的作用机制。方法：采用冠状动脉结扎法复制心室重构大鼠模型,造模2周后将模型大鼠随机分为模型组,卡托普利4.4 mg.kg-1组,苓桂术甘汤（按生药量计）低、中、高剂量（2.1,4.2,8.4 g.kg-1）组,另设假手术组,分别ig给药,连续给药4周,采用Western blot,RT-PCR及ELISA技术检测各组大鼠心肌组织NF-κB,NF-κB mRNA表达,血清NF-κB含量。结果：假手术组,模型组,苓桂术甘汤低、中、高剂量组,卡托普利组的心肌组织NF-κB相对表达量（NF-κB/β-actin）分别为：0.190±0.011,0.772±0.026,0.366±0.059,0.295±0.033,0.235±0.013,0.341±0.023;NF-κB mRNA相对表达量分别为：1.000,26.875,6.574,4.340,1.194,5.540;血清NF-κB含量分别为（125.85±14.76）,（196.98±17.79）,（163.89±20.08）,（131.73±10.47）,（141.93±10.32）,（133.93±9.27）ng.L-1。模型组与假手术组比心肌组织NF-κB,NF-κB mRNA表达、血清NF-κB含量均显著升高（P〈0.01）;苓桂术甘汤各剂量组及卡托普利组能够显著抑制模型大鼠心肌组织NF-κB,NF-κB mRNA表达、降低模型大鼠血清NF-κB含量,与模型组比有显著性差异（P〈0.01或P〈0.05）。结论：苓桂术甘汤干预AMI后VR的机制与其抑制NF-κB有关。

英文摘要：

Objective： To study the mechanism of Linggui Zhugan decoction （LGZGD） interference on ventrieular remodeling （VR） in rats after acute myocardial infarction （AMI） , through observing the expression of nuclear factor-KB （NF-KB） and NF-KB mRNA of myocardial tissue and the content of NF-KB in ventricular remodeling rats with AMI. Method： AMI model was produced by ligation of coronary artery. 2 weeks after modeling, rats were randomly classified into model, captopril, and low （2. 1 g -kg-1 ） , middle （4.2 g -kg-X ） and high （8.4 g ~ kg-1） dosage of LGZGD group. Control group and the other 5 groups were administered medications intragastrieally for 4 consecutive weeks. The content of NF-KB in myocardial tissue and serum was detected by ELISA and the expression of NF-KB was assayed by RT-PCR and the expression of NF-KB mRNA by Western blot. Result： For sham-operation, model, low, middle and large dosage of LGZGD group and captopril group, the content of NF-KB of myocardial tissue was 0. 190 ＋_0. 011, 0. 772 ＋-0. 026, 0. 366 ＋0. 059, O. 295 ~ 0. 033, 0. 235 ＋0. 013, 0. 341 ＋0. 023. The relative expression of NF-KB mRNA were 1. 000, 26. 875, 6. 574, 4. 340, 1. 194, 5. 540. The content of serum NF-KB were （ 125.85 ＋ 14.76） , （ 196.98 ＋_ 17.79） , （ 163.89 ＋ 20.08）, （131.73-＋10.47）, （141.93_＋10.33）, （133.93_＋9.27） ng- L-1. The content of NF-KB in）serum and the expression of NF-KB, NF-KB mRNA of myocardial tissue of model group increased significantly compared with control group （P 〈 O. O1 ）. Low, middle and high dosage of LGZGD and captopril group could decrease the content of NF-KB in serum and inhibited the expression of NF-KB, NF-KB mRNA in myocardial tissue of model rats significantly compared with model group （P 〈 O. 01 or P 〈 0.05）. Conclusion： The mechanism Of LGZGD interference VR of post-AMI seems to be related to the inhibition of NF-kB.