摘要
目的观察肝细胞生长因子(HGF)抑制急性心肌梗死后心肌氧化损伤的作用,并探讨其可能的机制。方法结扎犬冠状动脉前降支制造心肌梗死模型,给予心肌内注射HGF裸质粒干预。4周后,测定HGF在心肌的表达,测量心脏质量指数、心肌及血液中总超氧化物歧化酶(SOD)、铜锌-超氧化物歧化酶(CuZn-SOD)活性,血液过氧化氢(H2O2)含量,并与假手术组比较。结果心肌梗死组(M组)大鼠右室心脏质量指数(RVWI)、左室心脏质量指数(LVWI)升高(P<0.01),心肌、血液中SOD及CuZn-SOD活性下降,H2O2含量升高(P<0.01)。HGF组较M组RVWI、LVWI下降(P<0.01),血清和心肌SOD及CuZn-SOD活性升高,H2O2含量下降。结论 HGF改善急性心肌梗死后心室重塑和心功能,可能与其提高SOD活性抗氧化损伤有关。
Objective To investigate the effects of HGF abating oxidative damage after myocardium infarction and the possible mechanisms.Methods HGF was given to the dogs with myocardiac infarction by left anterior decending coronary artery ligation.After 4 weeks,expression of HGF was observed.The activity of superoxide dismutase（SOD） and copper-zinc SOD（CuZu-SOD） in left ventricular and hydrogen peroxide（H2O2） in serum were measured.Cardiac remodeling was observed through right ventricular weight index（RVWI）、left ventricular weight index（LVWI）.Results In the dog model of myocardiac infarction,The activity of SOD、CuZu-SOD in left ventricular decrease and H2O2 in serum increased.HGF gene therapy can simultaneously attenuate RVWI,LVWI（P〈0.01）,enhance SOD、CuZu-SOD activity and decrease content of H2O2 in serum（P〈0.01）.Conclusion The HGF gene can enhance activity of SOD、CuZu-SOD and improve cardiac remodeling after acute myocardiac infarction.
出处
《重庆医学》
CAS
CSCD
北大核心
2010年第11期1370-1371,1374,共3页
Chongqing medicine
