丹参酮ⅡA对心肌梗死模型大鼠心肌钙调蛋白及心功能的影响

Effect of tanshinone IIA on the calmodulin and heart function of the rats with acute ;myocardial infarction

目的：观察丹参酮ⅡA对心肌梗死模型大鼠心肌钙调蛋白（cardiac muscle, CaM）及钙调蛋白依赖性蛋白激酶Ⅱ（calcium/calmodulin-dependentproteinkinase-Ⅱ, CaMKⅡ）mRNA 表达和心功能的影响。方法100只大鼠按随机数字表法分为假手术组、模型组、丹参酮ⅡA组。模型组、丹参酮ⅡA组采用结扎左侧冠状动脉前降支45 min再灌注45 min，并反复3次阻断与再灌注的方法建立大鼠心肌梗死模型。丹参酮ⅡA组尾静脉注射丹参酮ⅡA磺酸钠注射液10 mg/kg，假手术组、模型组尾静脉注射等体积生理盐水。连续给药7 d后断头处死，取心脏用Langendorff离体心脏灌流器灌流离体心脏，测定各组大鼠给药前后离体心脏左室最大上升/下降速率（±LVdp/dtmax）、心肌收缩张力、心率等心功能指标；TTC染色观察心肌梗死面积；检测缺血区心肌组织CaM及CaMKII mRNA表达。结果与模型组比较，丹参酮ⅡA 组 CaM mRNA[（1.29±0.19）比（2.31±0.21）]及 CaMKⅡ mRNA[（1.10±0.07）比（2.13±0.18）]表达下调（P＜0.05），心肌梗死范围[（25.12±0.43）%比（35.15±0.64）%]缩小（P＜0.05），心肌收缩张力[（2.03±0.14）g比（1.06±0.12）g]及±LVdp/dtmax[（4701.2±135.3）mmHg/s比（3214.7±110.2）mmHg/s；（2518.7±65.4）mmHg/s比（1960.3±62.5）mmHg/s]增高（P＜0.05）。结论丹参酮ⅡA可下调急性心肌梗死模型大鼠心肌细胞CaM、CaMKⅡ mRNA表达，对心肌缺血有保护作用。

Objective To observe the effect of tanshinone IIA on the myocardial calmodulin （CaM） and calmodulin dependent protein kinase II （CaMK） mRNA expression and heart function of acute myocardial infarction rats. Methods A total of 100 rats were randomly divided into the sham operation group, the model group, and the tanshinone ⅡA group. The model of acute myocardial infarction was established by the ligation of left anterior descending coronary artery ligation with 45 min, and reperfusion with 45 min, and the above process was repeated 3 times. Tanshinone IIA group was treated with intravenous injection of 10 mg/kg sodium tanshinone ⅡA, while the sham operation group and the model group with 10 mg/kg saline, and all treatment last 7 days. The mRNA expressions of CaM and CaMKII were determined. TTC staining was used to observe areas of myocardial infarction. The left ventricular maximum rise/fall rate （±LVdp/dtmax）, myocardial contraction tension, heart rate and heart function index were detected pre-and post-treatment by the Langendorff device perfusion of isolated heart. Results Compared with the model group, the mRNA expression of and CaM mRNA （1.29 ± 0.19 vs. 2.31 ± 0.21） and CaMK II （1.10 ± 0.07 vs. 2.13 ± 0.18） in the tanshinone IIA group were significantly lower （P〈0.05）, and the areas of myocardial infarction （25.12%± 0.43%vs. 35.15%± 0.64%）＆amp;nbsp;significantly decreased （P〈0.05）, and the IT （2.03 ± 0.14 g vs. 1.06 ± 0.12 g）, the ±LV dp/dtmax （4 701.2 ± 135.3 mmHg/s vs. 3 214.7 ± 110.2 mmHg/s, 2 518.7 ± 65.4 mmHg/s vs.1 960.3 ± 62.5 mmHg/s） significantly increased （P〈0.05）. Conclusion Tanshinone IIA may protect myocardial ischemia by regulating the mRNA expression of CaM and CaMKⅡ.