鸢尾苷元对急性心肌梗死小鼠心肌的保护作用

Cardioprotective function of tectorigenin in acute myocardial infarction in mice

目的观察鸢尾苷元对小鼠急性心肌梗死模型缺血心肌的影响,并探讨其作用机制。方法开胸结扎左冠状动脉前降支建立小鼠急性心肌梗死模型,分生理盐水组、复方丹参组、溶媒组、鸢尾苷元小剂量(5g·L-1)和大剂量组(10g·L-1),每组10只。观察各组心肌梗死面积、血清心肌酶、血清过氧化物歧化酶(SOD)和丙二醛(MDA)含量,及缺血心肌血管内皮生长因子A(VEGFa)、内皮型一氧化氮合成酶(eNOS)和β-肾上腺素受体激酶1(β-ARK1) mRNA的表达。结果与生理盐水组相比,鸢尾苷元组心肌梗死面积明显缩小(P<0.01),血清心肌酶和MDA含量降低(P<0.01)。心肌VEGFa和eNOS mRNA的表达上调(P<0.01),β-ARK1 mRNA的表达下调(P<0.01),且随着剂量的增加其作用加强。结论鸢尾苷元对急性心肌梗死小鼠心肌有明显的保护作用,其作用机制与其抗氧化损伤及上调VEGFa和eNOS mRNA的表达、下调β-ARK1的表达有关。

AIM To observe the protective effects of tectorigenin on ischemic myocardium model. METHODS The acute myocardial infarction model was established by ligating the left anterior descending coronary artery in the Kunming-strain mouse. The mice were administered with normal saline （group A）, Danshen （group B）, vehicle （group C）, low-dose tectorigenin （group D）, high-dose tectorigenin （group E）,respectively. The myocardial infarct area was evaluated by observing the changes in histology. Serum concentration of myocardial enzyme, SOD and MDA were determined by test kits. The expression of vascular endothelial growth factor A （VEGFa）, endothelium nitric oxide synthetase （eNOS） and β-adrenergic receptor kinase （β-ARK1） were determined by real-time PCR. RESULTS Compared with the group A, the myocardial infarct area was significantly lower （P 〈 0.01） in the group D and E （P 〈 0.01 ）. The serum concentrations of myocardial enzyme and MDA decreased significantly （P 〈 0.01 ） . The expressions of VEGFa and eNOS were upregulated, and the expression of β-ARK1 was downregulated （P 〈 0.01） . And the protective effect of tectorigenin increased in a dose-dependent manner. CONCLUSION Tectorigenin could protect the ischemic myocardium in acute myocardial infarction mouse through preventing oxidation, upregulating the expressions of VEGFa and eNOS, and downregulating the expression of β-ARK1.