蓝莓花色苷预处理对大鼠心肌梗死的保护作用

目的观察蓝莓花色苷（blueberryanthocyanin，BBA）预处理对实验性急性心肌梗死大鼠心肌梗死面积，心肌肌钙蛋白-T（cTn-T）表达，Bax、Bcl-2mRNA表达的影响，探讨其干预心肌梗死的机制。方法40只Wistar大鼠随机分为假手术组，心肌梗死模型组，BBA低、中、高剂量组，药物干预4周，末次给药30min后结扎左冠状动脉前降支建立心梗动物模型。24h后，TTC检测心肌梗死面积；Westernblotting方法检测心肌细胞cTn-T蛋白表达；realtimePCR方法检测Bcl-2mRNA、BaxmRNA表达。结果模型组和假手术组相比，模型组心肌梗死面积显著升高（P〈0．01），心肌细胞cTn．T蛋白表达下降（P〈0．05），Bcl-2mRNA表达下降（P〈0．05），BaxmRNA表达显著升高（P〈0．01），Bcl-2／Bax比值显著降低（P〈0．01）。BBA干预给药组和模型组相比，中剂量组心肌梗死面积低于模型组（P〈0．05），低剂量组心肌细胞cTn-T蛋白表达升高（P〈0．05），中剂量组Bcl-2mRNA表达升高（P〈0．05），低、中剂量组BaxmRNA表达下降（P〈0．05），中剂量组Bcl-2／Bax比值升高（P〈0．05）。结论蓝莓花色苷对心肌梗死后心肌细胞具有明确的保护作用，其机制可能与减少心肌梗死面积，上调心肌细胞eTn-T蛋白的表达，上调Bcl-2mRNA表达、下调BaxmRNA表达，抑制心肌梗死后心肌细胞凋亡有关。

Protective effect of blueberry anthocyanins pretreatment on myocardial infarction in rats

Objective To observe the effect of blueberry anthocyanins （BBA） pretreatment on experimental acute myocardial infarction area in rats and cardiac troponin-T （cTn-T） expression, expression of Bax and Bcl-2 mRNA, and explore the intervention mechanism of myocardial infarction. Methods Forty Wistar rats were randomly divided into sham operation group （sham）, myocardial infarction model group （MI）, BBA low- （BBA 100 mg/kg.d）, medium- （BBA 200 mg/kg.d） , and high-dose group （BBA 400 mg/kg-d）. Drug intervention was given for 4 weeks. At 30 minutes after the last administration, the left anterior descending branch of coronary artery was ligated to establish myocardial infarction animal models. Myocardial infarction area was detected by TTC test 24 hours later. Western blotting was used to detect the cTn-T protein expression in myocardial cells. Expression of Bcl-2 and Bax mRNA was detected by real time PCR. Results Compared with that of the sham group, the myocardial infarction area in the MI group was significantly larger （P 〈 0. {）1 ） , expression of eTn-T protein in myocardial cells was significantly lower （P 〈 0. 05） , the Bcl-2 mRNA expression wassignificantly decreased （ P 〈 0..05 ） , expression of Bax mRNA was significantly increased （ P 〈 0. 01 ） , and Bcl-2/Bax ratio was significantly decreased （P 〈 0.01 ） in the MI group. Compared with the MI group, the myocardial infarction area in the BBA 200 group was significantly lower than that of the MI group （ P 〈 0. 05 ）, expression of myocardial cell cTn-t protein was increased in the BBA 100 gr0up （ P 〈 0.05 ）, Bcl-2 mRNA expression was increased in the BBA 200 group （ P 〈 0.05 ）, Bax mRNA expression was decreased in the BBA 200 and BBA 100 groups （ P 〈 0.05 ）, and Bcl-2/Bax ratio was increased in the BBA 200 group （ P 〈 0.05 ）. Conclusions Blueberry anthocyanins clearly show protective effect on myocardial cells after myocardial infarction. Its mechanism may be related with reducing the myocardial infarction area, up- regulation of the expression of cTn-T protein and Bcl-2 mRNA, down-regulation of Bax mRNA expression, and inhibit apoptosis in myocardial cells after myocardial infarction.