文献类型：期刊文献

中文题名：当归黄芪超滤物对电离辐射诱导下心肌细胞的影响及其机制研究

英文题名：Effect of Angelica astragalus ultrafiltration on cardiomyocytes induced by ionizing radiation and its mechanism

作者：王夏颖[1];蒋虎刚[1,2];刘佳坤[1];马静[1];刘凯[1,2];李应东[1,2];赵信科[1,2]

第一作者：王夏颖

机构：[1]甘肃中医药大学,兰州730000,甘肃;[2]甘肃中医药大学附属医院,兰州730000,甘肃

第一机构：甘肃中医药大学

年份：2026

卷号：31

期号：3

起止页码：300

中文期刊名：中国临床药理学与治疗学

外文期刊名：Chinese Journal of Clinical Pharmacology and Therapeutics

收录：;北大核心:【北大核心2023】；

基金：国家自然科学基金资助项目(82360926);甘肃省教育厅:优秀研究生“创新之星”项目(2025CXZX-939.);甘肃中医药大学研究生创新基金资助项目(2025CXCY-007)。

语种：中文

中文关键词：放射性心脏损伤;当归黄芪超滤物;电离辐射;心肌细胞

外文关键词：radiation-induced heart injury;radix angelicae sinensis and radix hedysari;ionizing radiation;cardiomyocytes

摘要：目的:探究电离辐射对H9C2心肌细胞的影响及当归黄芪超滤物(RAS-RH)的干预效应。方法:应用X射线建立H9C2损伤模型,并选用RAS-RH对其进行干预。通过CCK-8法检测各组H9C2的活力情况,鬼笔环肽染色观察细胞的肌丝骨架变化,JC-1染色及流式细胞术检测细胞线粒体膜电位(ΔΨm)变化,Hoechst33324染色及流式细胞术检测细胞的凋亡情况,蛋白免疫印迹法(Western blot)实验检测Drp1和HSP70相关蛋白的表达水平。结果:(1)X射线可抑制H9C2的增殖(P<0.05),破坏细胞肌丝骨架、降低细胞活力、改变ΔΨm以及促进细胞凋亡(P<0.01,P<0.05);(2)RAS-RH干预后H9C2活力升高(P<0.01)、细胞肌丝骨架恢复,且细胞的增殖能力、ΔΨm以及细胞凋亡(P<0.01、P<0.05)均得以改善;(3)RAS-RH可通过调节Drp1及HSP70蛋白的相对表达量(P<0.05)来改善H9C2生物学功能。结论:电离辐射通过破坏细胞肌丝骨架、降低细胞活力、下调ΔΨm以及促进细胞凋亡进程来破坏H9C2的生物学功能,而RAS-RH可通过调节Drp1及HSP70蛋白的相对表达水平以修复电离辐射所带来的H9C2损伤。
AIM:To investigate the effects of ionizing radiation on H9C2 cardiomyocytes and the intervention efficacy of Radix Angelicae Sinensis-Radix Astragali ultrafiltrate(RAS-RH).METHODS:An H9C2 cardiomyocyte injury model was established using X-ray irradiation,followed by intervention with RAS-RH.Cell viability was assessed using the CCK-8 assay.Phalloidin staining was employed to observe changes in the cytoskeletal structure of cardiomyocytes.JC-1 staining combined with flow cytometry was used to measure mitochondrial membrane potential(ΔΨm).Hoechst 33324 staining and flow cytometry were applied to evaluate apoptosis.Western blot was performed to determine the expression levels of Drp1 and HSP70 proteins.RESULTS:(1)X-ray irradiation significantly inhibited the proliferation of H9C2 cells(P<0.05),disrupted cytoskeletal integrity,reduced cell viability,altered mitochondrial membrane potential(ΔΨm),and promoted apoptosis(P<0.01,P<0.05).(2)Intervention with RAS-RH(Radix Astragali and Radix Angelicae Sinensis ultrafiltrate)markedly enhanced H9C2 cell viability(P<0.01),restored cytoskeletal organization,and improved proliferative capacity,ΔΨm,and apoptosis resistance(P<0.01,P<0.05).(3)Mechanistically,RAS-RH ameliorated H9C2 cell function by modulating the relative protein expression levels of Drp1(Dynamin-related protein 1)and HSP70(Heat shock protein 70)(P<0.05).CONCLUSION:Ionizing radiation impairs the biological function of H9C2 cardiomyocytes by disrupting the cytoskeletal structure,reducing cell viability,downregulatingΔΨm,and promoting apoptosis.In contrast,RAS-RH can mitigate radiation-induced cardiomyocyte damage by regulating the relative expression levels of Drp1 and HSP70 proteins.