丙酮酸脱氢酶激酶 shRNA 恢复心肌梗死 引起心脏功能紊乱的基础研究

Basic Study of Pyruvate Dehydrogenase Kinase shRNA in Restoring Cardiac Dysfunction Caused by Myocardial Infarction

摘要:

〔摘 要〕 目的：探讨丙酮酸脱氢酶激酶（PDHK）短发卡状核糖核酸（shRNA）恢复心肌梗死引起心脏功能紊乱 的价值。方法：取无特定病原体（SPF）级 Wistar 大鼠 40 只，按照随机数字表法分为两组，观察组为转染 PDHK4 shRNA 的心肌细胞，对照组为普通心肌细胞。比较心肌细胞是否转染 PDHK4 shRNA 的生存能力；观察转染 PDHK4 shRNA 与心肌和心脏功能恢复情况。结果：培养 1 周时，观察组大鼠的生存率达到 90.0 %，对照组生存率仅 50.0 %。 培养 1 周内观察组 PDHK4、PDH 表达量低于对照组，培养 4 周内，观察组 H+ 水平和乳酸产生量低于对照组，左心 室射血率高于对照组，梗死面积小于对照组，差异均具有统计学意义（P ＜ 0.05）。结论：心肌梗死的心肌细胞在转 染 PDHK shRNA 后，生存能力增强，PDHK shRNA 转染入心脏后，PDHK 表达被抑制，进而降低心肌纤维化程度， 促进心脏功能的恢复，达到提高模型动物生存率的目的。

Abstract:

〔Abstract〕Objective To investigate the value of pyruvate dehydrogenase kinase (PDHK) and short hairpin ribonucleic acid (shRNA) in restoring cardiac dysfunction caused by myocardial infarction. Methods 40 specific pathogen free (SPF) Wistar rats were divided into two groups according to the random number table method. The observation group was PDHK4 shRNA transfected cardiomyocytes, and the control group was ordinary cardiomyocytes. The viability of myocardial cells transfected with PDHK4 shRNA was compared. PDHK4 shRNA transfected with myocardial and cardiac function recovery were observed. Results After 1 week of culture, the survival rate of rats of the observation group was 90.0 %, while that of the control group was only 50.0 %. The expression levels of PDHK4 and PDH in the observation group were lower than those in the control group within 1 week of culture, the H+ level and lactic acid production in the observation group were lower than those in the control group within 4 weeks of culture, the left ventricular ejection rate was higher than that in the control group, and the infarct area was smaller than that in the control group, the difference was statistically significant (P < 0.05). Conclusion The viability of myocardial cells with myocardial infarction is enhanced after transfection of PDHK shRNA. After transfection of PDHK shRNA into heart, the expression of PDHK was inhibited, and then the degree of myocardial fibrosis was reduced, the recovery of cardiac function was promoted, and the survival rate of model animals was improved.