以Notch-1信号系统为靶点干预对高糖诱导的大鼠胚胎心肌细胞H9C2增殖、凋亡及纤维化的影响  

Effect of Notch-1 signaling system as a target intervention on prolifera-tion,apoptosis and fibrosis of H9C2 induced by high glucose in rat em-bryonic cardiomyocytes

作　　者：张健 吴艳 魏友平 涂晓文 ZHANG Jian;WU Yan;WEI Youping;TU Xiaowen(Department of Cardiovascular Medicine,Jiangxi Integrated Traditional Chinese and Western Medicine Hospital,Jiangxi Province,Nanchang 330000,China)

机构地区：[1]江西省中西医结合医院心血管内科,江西南昌330000

出　　处：《中国当代医药》2025年第11期4-8,共5页China Modern Medicine

基　　金：江西省卫生健康委科技计划项目(202311252)。

摘　　要：目的探讨以Notch-1信号系统为靶点干预对高糖诱导的大鼠胚胎心肌细胞H9C2增殖、凋亡及纤维化的影响。方法将H9C2心肌细胞随机分为6组,即正常对照组、甘露醇高渗对照组、阳性对照组、抑制剂组、Notch-1组、空载体组。在上述各组培养完成后,检测各组H9C2心肌细胞的增殖抑制率、凋亡率、磷脂酰肌醇3激酶(PI3K)和蛋白激酶B(AKT)mRNA表达、Notch-1、磷酸化磷脂酰肌醇3激酶(p-PI3K)/磷酸化蛋白激酶B(p-AKT)蛋白表达情况。结果阳性对照组、抑制剂组、空载体组的增殖抑制率、凋亡率均高于Notch-1组,差异有统计学意义(P<0.05);Notch-1组的PI3K、AKT mRNA表达水平均高于其他各组,且Notch-1组的Notch-1、p-PI3K/p-AKT蛋白表达水平均高于其他各组,差异有统计学意义(P<0.05)。结论高糖将抑制H9C2心肌细胞的增殖率,Notch-1作为心肌损伤的保护因子,以PI3K/AKT作为立足点,能够干预糖尿病心肌病增殖、凋亡及纤维化进程,促进H9C2心肌细胞增殖,为糖尿病心肌病治疗提供了新的靶点。Objective To investigate the effect of Notch-1 signaling system as a target intervention on proliferation,apoptosis and fibrosis of H9C2 induced by high glucose in rat embryonic cardiomyocytes.Methods H9C2 cardiomyocytes were randomly divided into 6 groups,namely normal control group,mannitol hypertonic control group,positive control group,inhibitor group,Notch-1 group and empty carrier group.After culture in the above groups,the proliferation inhibition rate,apoptosis rate,phosphatidylinositol 3 kinase(PI3K)and protein kinase B(AKT)mRNA expression,Notch-1,phosphorylated-phosphatidylinositol 3 kinase(p-PI3K)/phosphorylated-protein kinase B(p-AKT)protein expression of H9C2 cardiomyocytes in each group were detected.Results The proliferation inhibition rate and apoptosis rate of positive control group,inhibitor group and empty carrier group were higher than those of Notch-1 group,and the differences were statistically significant(P<0.05).The mRNA expression levels of PI3K and AKT in Notch-1 group were higher than those in other groups,and the protein expression levels of Notch-1 and p-PI3K/p-AKT in Notch-1 group were higher than those in other groups,with statistically significant differences(P<0.05).Conclusion High glucose can inhibit the proliferation rate of H9C2 cardiomyocytes.Notch-1,as a protective factor of myocardial injury,can intervene in the proliferation,apoptosis and fibrosis process of diabetic cardiomyopathy with PI3K/AKT as a foothold,and promote the proliferation of H9C2 cardiomyocytes,providing a new target for the treatment of diabetic cardiomyopathy.

关 键 词：糖尿病心肌病 Notch同源物1 信号系统 保护作用 

分 类 号：R541[医药卫生—心血管疾病]