黄芪甲苷对辐射诱导的大鼠H9C2心肌细胞凋亡及miR-134-5p/BDNF/PI3K信号通路的影响OA
Effects of Astragaloside Ⅳ on Radiation-Induced Apoptosis of H9C2 Cardiomyocytes in Rats and miR-134-5p/BDNF/PI3K Signaling Pathway
目的:探讨黄芪甲苷对辐射引起的心肌细胞损伤凋亡的防护作用及相关机制.方法:将 H9C2 细胞分为空白对照组、模型对照组(6 Gy X 线辐照)、黄芪甲苷 6 μg/mL 组(照射前预处理细胞);采用 CCK-8 法检测细胞存活率;DCFH-DA 探针检测活性氧(ROS)水平;试剂盒测定超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量;JC-1 法检测线粒体膜电位;Annexin V-FITC/PI 双染流式和 Hoechst 33342 染色检测细胞凋亡率;qRT-PCR 法检测miR-134-5p 表达;Western blot 法检测细胞BDNF、PI3K、AKT、p-AKT、BCL-2、BAX 蛋白表达.结果:与空白对照组比较,模型对照组细胞 ROS 水平和 MDA 含量升高,SOD 活力下降,线粒体膜电位下降百分率升高,细胞凋亡率明显增加,miR-134-5p 表达上调,细胞 BDNF、PI3K 及 p-AKT、BCL-2 等蛋白表达下调,BAX 蛋白表达上调(P<0.05);与模型对照组相比,黄芪甲苷6 μg/mL 组细胞 ROS 水平和 MDA 含量降低,SOD 活力升高,线粒体膜电位百分率降低,细胞凋亡率下降,miR-134-5p 表达下调,细胞 BDNF、PI3K、p-AKT、BCL-2 蛋白表达上调,BAX 表达下调(P<0.05).结论:黄芪甲苷能减轻辐照导致的心肌细胞氧化应激和线粒体损伤,减少细胞凋亡,其防护作用与黄芪甲苷调控 miR-134-5p/BDNF/PI3K 信号通路有关.
Objective:To explore the protective effects and related mechanisms of Astragaloside Ⅳ(ASⅣ)on ra-diation-induced cardiomyocyte injury and apoptosis.Methods:H9C2 cells were divided into a normal control group,a model control group(6 Gy X-ray irradiation),and an ASⅣ 6 μg/mL group(cells pretreated before irradiation).Cell viability was detected using the CCK-8 assay.Reactive oxygen species(ROS)levels were detected with DCFH-DA probes.Superoxide dismutase(SOD)activity and malondialdehyde(MDA)content were measured with commercial kits.Mitochondrial membrane potential was assessed by the JC-1 method.Apoptosis rate was detected by Annexin V-FITC/PI double staining flow cytometry and Hoechst 33342 staining.MiR-134-5p expression was determined by qRT-PCR.BDNF,PI3K,AKT,p-AKT,BCL-2,and BAX protein expression was analyzed by Western blot.Results:Compared with the normal control group,the model control group showed increased ROS levels and MDA content,decreased SOD activity,an increased percentage of mitochondrial membrane potential loss,significantly increased apoptosis rate,upregu-lation of miR-134-5p,downregulation of BDNF,PI3K,p-AKT,and BCL-2 protein expression,and upregulation of BAX expression(P<0.05).Compared with the model control group,the ASⅣ 6 μg/mL group showed reduced ROS levels and MDA content,increased SOD activity,a decreased percentage of mitochondrial membrane potential loss,reduced ap-optosis rate,downregulation of miR-134-5p,upregulation of BDNF,PI3K,p-AKT,and BCL-2 protein expression,and downregulation of BAX expression(P<0.05).Conclusion:ASⅣ can attenuate oxidative stress and mitochondrial dam-age induced by irradiation and reduce cardiomyocyte apoptosis.Its protective effect is associated with regulation of the miR-134-5p/BDNF/PI3K signaling pathway.
顾静;荆爽;韩晓斐;方丹;董晓丽;颉亚辉
甘肃中医药大学基础医学院,兰州 730000甘肃中医药大学基础医学院,兰州 730000甘肃中医药大学基础医学院,兰州 730000甘肃中医药大学基础医学院,兰州 730000甘肃中医药大学基础医学院,兰州 730000甘肃中医药大学数学与卫生统计学教研室,兰州 730000
黄芪甲苷辐射损伤心肌细胞微小核糖核酸-134-5p细胞凋亡
Astragaloside ⅣRadiation injuryCardiomyocytesMicroRNA-134-5pApoptosis
《中药药理与临床》 2026 (6)
59-66,8
国家自然科学基金(编号:82360878).
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