Abstract: Abstract: Objective To investigate the effects of benzoylpaeoniflorin on cardiac function in rats with acute myocardial infarction ( AMI) through Nrf2 / HO-1 pathway. Method Thirty six SD rats were randomly divided into the sham group, the AMI group and the AMI +BA group. Rats in the AMI group and the AMI + BA group were established as AMI models. After modelling, rats in the AMI + BA group were given gavage with BA at the dose of 170 mg / kg. The electrocardiogram and myocardial enzymes creatine kinase MB ( CK-MB ) and lactate dehydrogenase ( LDH) of rats in each group were detected. Echocardiography detects cardiac function. HE staining and TUNEL staining were used to detect tissue damage and cardiomyocyte apoptosis. Western blot was used to detect protein levels in Nrf2 / HO-1 pathway. Result The levels of LVEF and ( ±dp / dtmax) in the AMI group were significantly lower than those in the sham group ( P < 0. 05) . The levels of LVEF and ( ± dp / dtmax) in the AMI+BA group were significantly higher than those in the AMI group ( P < 0. 05) . CK-MB and LDH in the sham group were significantly higher than those in the control group ( P < 0. 05) . CK-MB and LDH in AMI + BA group were significantly lower than those in the AMI group ( P < 0. 05) . The apoptosis rate in the AMI group ( 13. 08 ±1. 23) % was significantly higher than that in the sham group ( 1. 14 ± 0. 10 ) %, P < 0. 05. The cardiomyocyte apoptosis rate (6. 43±0. 78) % in the AMI + BA group was significantly lower than that in the AMI group,P<0. 05. Compared with the sham group, the levels of Nrf2 / HO-1 in the AMI group were significantly reduced,P<0. 05. The levels of Nrf2 / HO-1 in the AMI + BA group were significantly higher than those in the AMI group, P<0. 05. Conclusion BA inhibits myocardial cell apoptosis in AMI model rats by promoting the Nrf2 / HO-1 pathway and plays a role in protecting heart function.

Key words: Key words:acute myocardial infarction, benzoylpaeoniflorin, cardiac function, apoptosis, Nrf2 / HO-1 pathway

摘要： 摘要:目的 探究苯甲酰芍药苷( benzoylpaeoniflorin,BA) 通过核因子 E2 相关因子 2 / 血红素加氧酶 1( Nrf2 / HO-1)通路对急性心肌梗死( AMI)大鼠心功能的影响作用机制。 方法 36 只 SD 大鼠随机分为 3 组( n = 12) :Sham 组、AMI 组和 AMI+BA 组。 AMI 组和 AMI+BA 组大鼠建立 AMI 模型,建模后 AMI + BA 组大鼠使用 BA 灌胃,剂量为170 mg / kg。 检测各组大鼠心电图和心肌酶肌酸激酶 MB( CK-MB)和乳酸脱氢酶( LDH) 。 超声心动图检测心功能。HE 染色和 TUNEL 染色检测组织损伤和心肌细胞凋亡。 Western blot 检测 Nrf2 / HO-1 通路中蛋白水平。 结果 AMI组大鼠左室射血分数 ( LVEF) 及左室内压力最大变化率 ( ± dp / dtmax) 显著低 于 Sham 组 ( P < 0. 05) , AMI + BA 组LVEF 和±dp / dtmax 显著高于 AMI 组( P< 0. 05) 。 Sham 组 CK-MB 和 LDH 显著高于对照组( P < 0. 05) ,AMI+BA 组CK-MB 和 LDH 显著低于 AMI 组( P< 0. 05) 。 AMI 组的凋亡率( 13. 08± 1. 23) % 显著高于 Sham 组( 1. 14± 0. 10) % ,P<0. 05,AMI + BA 组心肌细胞凋亡率 ( 6. 43 ± 0. 78) % , 显著低于 AMI 组 ( P < 0. 05) 。 与 Sham 组 比 较, AMI 组 Nrf2 / HO-1 水平显著降低( P<0. 05) ,AMI+BA 组 Nrf2 / HO-1 水平显著高于 AMI 组( P< 0. 05) 。 结论 BA 通过促进 Nrf2 / HO-1 通路抑制 AMI 模型大鼠的心肌细胞凋亡,并发挥保护心功能的作用。

关键词: 关键词:急性心肌梗死, 苯甲酰芍药苷, 心功能, 凋亡, Nrf2 / HO-1 , 通路