| 赵 黎,孙 媛,岳 媛,刘婷婷,姜 珊,高卫华.PKC βII特异性抑制剂LY333531减缓心肌梗死后心肌纤维化[J].,2017,17(17):3234-3237 |
| PKC βII特异性抑制剂LY333531减缓心肌梗死后心肌纤维化 |
| PKCβII Selective Inhibitor LY333531 Attenuates Myocardial Infarction Induced Fibrosis |
| 投稿时间：2016-10-09 修订日期：2016-11-17 |
| DOI：10.13241/j.cnki.pmb.2017.17.008 |
| 中文关键词: PKCβII LY333531 心脏重塑 心肌梗死 心力衰竭 心肌纤维化 |
| 英文关键词: PKCβII LY333531 Cardiac remodeling Myocardial infarction Heart failure Myocardial fibrosis |
| 基金项目:国家自然科学基金项目（81300956）；陕西省自然科学基础研究计划面上项目（2016JM3005） |
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| 中文摘要: |
| 摘要 目的：探讨蛋白激酶CβII(PKCβII)特异性抑制剂LY333531对心梗后大鼠心功能和心肌纤维化的保护作用。方法：利用左冠状动脉降支(LAD)结扎制备大鼠心梗模型，将手术4周后出现心衰的大鼠分为模型组(MF+NS)和治疗组(MF+LY333531)，分别给予生理盐水和LY333531(10 mg/kg/d)处理6周，检测各组大鼠体重和各项心功能指标，利用HE染色观察各组大鼠心肌组织形态变化，利用天狼星红染色观察心肌组织胶原沉积情况。结果：相对于模型组，LY333531处理组大鼠左心室缩短率(FS)明显改善(从21 %到35 %)。HE染色显示LY333531能够部分逆转心衰大鼠心室壁肥厚和心肌细胞宽度，天狼星红染色显示治疗组胶原蛋白沉积降低150 %。结论：使用LY333531选择性抑制PKCβII能够改善心梗后心力衰竭模型大鼠心脏功能和抑制心肌纤维化。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the protective effects of protein kinase C βII (PKCβII) selective inhibitor LY333531 on the myocardial fibrosis after myocardial infarction (MI). Methods: The left anterior descending (LAD) coronary artery of male Sprague-Daw- ley (SD) rats was occluded to induce MI. At four weeks after MI, rats with heart failure (HF) signs were treated with the LY333531 (3 mg/kg/day) or normal sodium (NS) for 6 weeks. The body weight and cardiovascular parameters were detected. Cardiomyocyte hypertro- phy was evaluated by haematoxylin and eosin (H&E) staining. Collagen deposition was evaluated by picrosirius red staining. Results: LY333531 treatment improved fractional shortening (from 21 % to 35 %) compared to control (NS). Mid-ventricle tissue sections stained with (H&E) showed that LY333531 treatment reduced wall thickness and cardiomyocyte width. Picrosirius red staining exhibited a 150 % decrease in collagen deposition in rat hearts treated with LY333531. Conclusion: Sustained selective inhibition of LY333531 in a post-MI HF rat model improves cardiac function and is associated with inhibition of pathological myocardial remodeling. |
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