杨梅素通过激活AKT信号通路抑制心肌梗死后心脏重构的研究  

Myricetin inhibits cardiac remodeling after myocardial infarction by activating AKT signal pathway

作　　者：邵玲[1] 周梦桥 熊涛[1] 邓长金[1] SHAO Ning;ZHOU Mengqiao;XIONG Tao;DENG Changjin(Department of Cardiology,Jingmen Municipal No.1 People′s Hospital,Jingmen,Hubei 448000,China)

机构地区：[1]湖北省荆门市第一人民医院心血管内科

出　　处：《重庆医学》2019年第11期1817-1821,共5页Chongqing medicine

摘　　要：目的探讨杨梅素是否能够保护小鼠心肌梗死后心脏重构以及可能的分子机制。方法采用冠状动脉左前降支结扎手术建立心肌梗死模型,将C57BL/6J小鼠分为对照组、模型组、低浓度杨梅素组(100mg·kg^-1·d^-1)和高浓度杨梅素组(300mg·kg^-1·d^-1)。杨梅素处理组在手术第3天起采用灌胃方法处理心肌梗死小鼠25d,观察小鼠死亡率;4周后采用超声心动图检测小鼠心功能;病理染色检测心肌梗死面积;RT-PCR检测心脏重构标志物;免疫印迹法检测改变的蛋白分子。结果MI术后4周,与对照组比较,模型组小鼠生存率降低(37%),心功能明显恶化,心肌肥厚程度增加,纤维化水平增加,心脏炎性反应增加,氧化应激水平增加;低浓度和高浓度杨梅素处理均能明显增加小鼠术后生存率(低浓度组58%;高浓度组61%),改善心功能,减少心肌梗死面积,降低心肌肥厚、纤维化、炎性反应、氧化应激水平;且高浓度杨梅素处理组效果优于低浓度杨梅素组;免疫印迹结果显示,杨梅素可增加PI3K、AKT和mTOR信号通路蛋白的激活,促进细胞存活。结论杨梅素可以通过激活AKT信号通路,改善心肌梗死后的心脏重构。Objective To investigate whether myricetin can protect the cardiac remodeling after myocardial infarction(MI) in mice and its possible molecular mechanism. Methods The left anterior descending coronary artery ligation was used to establish the myocardial infarction (MI) model.C57BL/6J mice were randomly divided into the control group,model group,low concentration of myricetin treatment group (100 mg·kg^-1 ·d^-1 ) and high concentration of myricetin treatment group (300 mg·kg^-1 ·d^-1 ).The myricetin treatment groups began to treat the mice with MI for 25 d on postoperative 3 d by using the gavage method.The death rate of mice was observed.The mice cardiac function was detected by echocardiography after 4 weeks.The pathological staining was used to assess the myocardial infarction area.RT-PCR was used to detect the cardiac remodeling markers.Western blot was used to detect the changed protein molecule. Results The mice survival rate at 4 weeks after MI operation was decreased (37%),the cardiac function was significantly deteriorated,myocardiac hypertrophy degree was increased,the fibrosis level was increased,the cardiac inflammatory reaction was increased,the oxidative stress level was increased;the treatment of low and high concentrations of myricetin all could obviously increase the postoperative survival rate (low concentration group:58%;high concentration group:61%),improved the cardiac function,decreased the myocardiac infarction area,reduced the myocardial hypertrophy,fibrosis,inflammatory reaction and oxidative stress level;moreover which in the high concentration myricetin treatment group was superior to that in the low concentration group;the Western blot results showed that myricetin increased the activation of PI3K,AKT,and mTOR signaling pathway and promoted the cellular survival. Conclusion Myricetin improves the cardiac remodeling after myocardial infarction by activating the AKT signaling pathway.

关 键 词：杨梅素 心肌梗死 心脏重构 PI3K/AKT信号通路 

分 类 号：R541[医药卫生—心血管疾病]