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目的利用心肌梗死后心力衰竭模型研究组织激肽释放酶(TK)和缓激肽(BK)改善心功能、抑制心肌纤维化的机制。方法冠状动脉结扎后1周,纯化的TK及BK连续皮下渗透给药4周,5周后处死动物。导管法检测各组动物的心功能,天狼红染色检测胶原的沉积,银染法测量心肌细胞的面积,免疫组织化学法检测Ⅰ、Ⅲ型胶原,W estern b lot-ting检测TGF-β1、Sm ad 2和phosph-Sm ad 2的表达,化学发光法检测一氧化氮(NO)和过氧化物的含量。结果TK及BK能明显改善心功能,对梗死面积无影响。治疗组胶原的沉积明显减少,细胞肥大减轻,TGF-β1、Smad的表达和磷酸化减少,NO的合成增加,过氧化物蓄积减轻。结论TK及BK对心肌梗死后的心力衰竭有治疗作用,抑制TGF-β1活化及过氧化物形成是主要的机制。
Objective To study the mechanisms of cardiac kinases and myocardial fibrosis by using tissue kallikrein (TK) and bradykinin (BK) in heart failure model after myocardial infarction. Methods One week after the coronary artery was ligated, the purified TK and BK were administered subcutaneously for 4 weeks. Animals were sacrificed 5 weeks later. The cardiac function of each group of animals was detected by catheterization method, the deposition of collagen was detected by Sirius red staining, the area of cardiomyocytes was detected by silver staining, the collagen type Ⅰ and Ⅲ were detected by immunohistochemistry, the expressions of TGF-β1, Sm ad 2 and phosph-Sm ad 2 expression, chemiluminescence detection of nitric oxide (NO) and peroxide content. Results TK and BK can significantly improve cardiac function, no effect on infarct size. In the treatment group, collagen deposition was significantly reduced, cell hypertrophy was reduced, TGF-β1, Smad expression and phosphorylation decreased, NO synthesis increased, peroxide accumulation reduced. Conclusions TK and BK have a therapeutic effect on heart failure after myocardial infarction. Inhibition of TGF-β1 activation and peroxide formation is the main mechanism.