CAJ | 학술논문

心力衰竭%曲美他嗪%炎症%氧化应激%腹主动脉缩窄法%酶联免疫吸附试验%实时定量聚合酶链反应%免疫组织化学法%放射免疫法%大鼠心力衰竭%麯美他嗪%炎癥%氧化應激%腹主動脈縮窄法%酶聯免疫吸附試驗%實時定量聚閤酶鏈反應%免疫組織化學法%放射免疫法%大鼠
심력쇠갈%곡미타진%염증%양화응격%복주동맥축착법%매련면역흡부시험%실시정량취합매련반응%면역조직화학법%방사면역법%대서
trimetazidine%heart failure%inflammation%oxidative stress%partially banding abdominal aortic artery%en-zyme-linked immunosorbent assay%Real-Time polymerase chain reaction%immunohistochemistry%radioimmunoassay%rat

目的：探讨曲美他嗪对心力衰竭大鼠抗炎、抗氧化应激作用。方法：采用腹主动脉缩窄法制备SD大鼠心力衰竭模型，双抗体夹心ELISA法检测血浆CRP、IL-6和TNF-α的表达水平；real-time PCR定量分析超氧化物歧化酶（SOD）、血红蛋白氧合酶（HO-1）、谷胱甘肽过氧化物酶（GPX）表达；免疫组织化学法检测SOD；放射免疫法检测总抗氧化能力（T-AOC）。结果：模型组血浆C反应蛋白、IL-6和TNF-α水平升高，曲美他嗪治疗组C反应蛋白、IL-6和TNF-α水平下降（P<0.01或0.05）；模型组SOD、GSH-Px、HO-1表达和T-AOC水平明显降低（P<0.01或0.05）。曲美他嗪治疗后，SOD、GPx、HO-1和T-AOC表达水平均有所升高，以SOD、T-AOC改善明显（P<0.05、P<0.01），高剂量组SOD表达甚至高过假手术组。结论：曲美他嗪能减少心衰大鼠模型炎症因子的表达，提高心肌氧化相关基因的表达，从而改善心功能。
목적：탐토곡미타진대심력쇠갈대서항염、항양화응격작용。방법：채용복주동맥축착법제비SD대서심력쇠갈모형，쌍항체협심ELISA법검측혈장CRP、IL-6화TNF-α적표체수평；real-time PCR정량분석초양화물기화매（SOD）、혈홍단백양합매（HO-1）、곡광감태과양화물매（GPX）표체；면역조직화학법검측SOD；방사면역법검측총항양화능력（T-AOC）。결과：모형조혈장C반응단백、IL-6화TNF-α수평승고，곡미타진치료조C반응단백、IL-6화TNF-α수평하강（P<0.01혹0.05）；모형조SOD、GSH-Px、HO-1표체화T-AOC수평명현강저（P<0.01혹0.05）。곡미타진치료후，SOD、GPx、HO-1화T-AOC표체수평균유소승고，이SOD、T-AOC개선명현（P<0.05、P<0.01），고제량조SOD표체심지고과가수술조。결론：곡미타진능감소심쇠대서모형염증인자적표체，제고심기양화상관기인적표체，종이개선심공능。
Objective:To Explore The anti-inflammatory and anti-oxidative stress of Trimetazidine(TMZ) in rats with heart failure. Methods: Rat models with congestive heart failure were achieved by partially banding the abdominal aortic arteries. The expression levels of plasma CRP, IL-6 and of TNF-α were detected by Double-antibody sandwich ELISA. The expression of superoxide dismutase(SOD), heme oxygenase( HO-1) and glutathione peroxidase(GPX) were measured by Real-Time PCR. SOD was detected by immunohistochemistry. T-AOC was detected by Radioimmunoassay Method. Re-sults:Compared with the Sham operation group, the CRP, IL-6 and TNF-αwere increased in the heart failure models, and were significantly decreased in the TMZ treatment group(P<0.01 or P<0.05). The SOD, GPX, HO-1 and T-AOC were sig-nificantly decreased in the heart failure models (P<0.01 or P<0.05) and increased in the TMZ treatment group,and SOD and T-AOC were especially increased (P<0.05, P<0.01). The activity of SOD of the high dose was higher than in the sham operation group. Conclusion:Trimetazidine can reduce the expression of inflammatory factors in rat models with heart fail-ure, and improve the myocardial oxidation-related gene expression, thereby improving cardiac functions.