中文摘要：

目的 探讨重组腺相火病毒（rAAV）介导血红素加氧酶-1（HO-1）基因转染对大鼠离体心脏缺血再灌注损伤时炎性细胞因子的影响：方法健康雄性SD大鼠30H，体重220～280g，随机分为3组：对照组（C组，Ⅳ=6）、生理盐水组（N组，n=12）和rAAV-HO-1组（H组，n=12）。N组和H组分别心叭注射600μl生理盐水或rAAV—HO-1（1．5×10 ^11v．g．）。基因转染后3个月，N组和H组各处死6只大鼠，取注射部位心肌组织，测定HO-1的表达制备大鼠离体心脏缺血再灌注模型，于平衡灌注15min）、阵灌注15、30、45min时，记录左心室舒张末压（LVEDP）、左心窜收缩压（LVSP）、丘心室收缩压最犬上升速率（＋dp／dtmax）和五心牵收缩压最大下降速牢（-dp/dtmax），测定心肌组织肿瘤坏死因子α（TNF-α）和自细胞介素6（IL-6）的含量。结果H组心肌组织HO-1表达较N组上调（P〈0．01）。与C组比较，N组和H组再灌注各时点LVEDP、心肌组织TNF-α和IL-6的含量升高，LYDP和±dp／dtmax、均降低（P〈0．05或0．01）；与N组比较，H组LVEDP、心肌组织TNF-α和IL-6的含量降低，LVSP和±dp／dtmax均升高（P〈0．05或0．01）．结论 rAAV介导HO—1基因转染大鼠心肌后，可减轻离体心脏缺血再灌注损伤，其机制与抑制炎性细胞因子的生成有关。

英文摘要：

Objective To investigate the effects of recombinant adeno-associated virus （rAAV）-mediated heine oxygenase-1（HO-1） gene transfer on inflammatory cytokine in isolated rat hearts with myocardial ischemiareperfusion （I/R） injury. Methods Thirty male SD rats weighing 220-280 kg were randomly divided into 3 grnups： group Ⅰ normal control （n = 6）; group Ⅱ normal saline ＋ I/R （n = 12） and group Ⅲ rAAV-HO-1 ＋ I/R （n = 12）. In group Ⅲ rAAV-mediated HO-1 was injected intramuscularly at 4 points on the anterior and posterior wall of left ventricle along the left anterior descending hranch of coronary artery. In group Ⅱ normal saline was injected instead of rAAV- HO-1 gene. Six animals in each group weer,.- saerificed 3 months alter the gene delivery in group Ⅱand Ⅲ.The expression of HO-1 in the injected myocardium was determined by immunohistochemical technique.The isolated rat hearts were perfused with an owygenated（95% O2-5% CO2）K-H solution at 37℃ in a Langendorff apparatus and subjected to 40 min of global ischemia followed by 45 min of reperfusion in group Ⅱand Ⅲ.The left ventricular diastolic pressure（LVDP）,left ventricular end-diastolic pressure（LVEDP）and±dp/dtmax were measured recorded at 15 min of post-preparation equilobration and at 15,30and45 min of reperfusion.TNF-α and IL-6 contents in myocardium were measured.Results The HO-1 expression was significantly higher in group Ⅲ than in group Ⅱ （ P 〈 0.05 or 0.01 ） . The left ventricular function was significantly better and TNF-α and IL-6 contents in myocardium were significantly lower in. group Ⅲ than in group Ⅱ （P 〈 0.05 or 0.01）.Conclusion rAAV-mediated HO-1 gene transfer can protect myocardium against I/R injury in isolated rat hearts through inhibition of inflammatory cytokine production.