放射性心脏病体外模型的构建策略与应用挑战

doi:10.12092/j.issn.1009-2501.2026.05.008

中国临床药理学与治疗学 ›› 2026, Vol. 31 ›› Issue (5): 639-648.doi: 10.12092/j.issn.1009-2501.2026.05.008

放射性心脏病体外模型的构建策略与应用挑战

王夏颖¹(), 蒋虎刚¹^,²^,³, 任春贞¹^,², 马静¹, 刘佳坤¹, 刘凯¹^,²^,³, 李应东¹^,²^,³, 赵信科¹^,²^,³^,*()

1. 甘肃中医药大学中西医结合学院，兰州 730000，甘肃
2. 甘肃省中医药防治慢性病重点实验室，兰州 730000，甘肃
3. 甘肃中医药大学附属医院，兰州 730000，甘肃

收稿日期:2025-06-29 修回日期:2025-09-03 出版日期:2026-05-26 发布日期:2026-06-02
通讯作者: 赵信科 E-mail:1686610858@qq.com;zxkd412@163.com
作者简介:王夏颖，女，在读硕士研究生，研究方向：中西医结合防治心血管疾病。E-mail：1686610858@qq.com
基金资助:
国家自然科学基金资助项目（82360926）；中医药传承与创新“百千万”人才工程（岐黄工程）青年岐黄学者基金资助项目；国家中医药管理局“李应东全国名中医传承工作室”建设项目（国中医药办人教函[2022]5号）；甘肃省科技重大专项计划（20ZD7FA002）；“双一流”科研重点项目（GSSYLXM-05）；甘肃省中医药科研课题项目（GZKZD-2018-02，GZKP-2023-59）；甘肃中医药大学第三附属医院院内课题（2022YK-11）；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）

Construction strategy and application of an in vitro model of radioactive cardiac injury

Xiaying WANG¹(), Hugang JIANG¹^,²^,³, Chunzhen REN¹^,², Jing MA¹, Jiakun LIU¹, Kai LIU¹^,²^,³, Yingdong LI¹^,²^,³, Xinke ZHAO¹^,²^,³^,*()

1. College of Integrated Traditional Chinese and Western Medicine, Gansu University of Chinese Medicine, Lanzhou 730000, Gansu, China
2. Gansu Provincial Key Laboratory of Traditional Chinese Medicine for Chronic Disease Prevention and Treatment, Lanzhou 730000, Gansu, China
3. Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou 730000, Gansu, China

Received:2025-06-29 Revised:2025-09-03 Online:2026-05-26 Published:2026-06-02
Contact: Xinke ZHAO E-mail:1686610858@qq.com;zxkd412@163.com

摘要/Abstract

摘要：

放射性心脏病（radiation-induced heart disease，RIHD）是胸部肿瘤放射治疗中最常见、最严重的并发症。心脏组织受到放射线的辐射后，出现心肌炎症、纤维化和血管内皮损伤等，进而引发心脏功能障碍。医疗水平的不断提升，大幅度延长了肿瘤患者的生存期，但是RIHD却严重影响了患者的生存质量。为了深入探究其病理机制，构建可靠的RIHD细胞模型是研究其分子机制和评估治疗效果的重要实验基础。本文总结了近年来国内外RIHD细胞模型在相关研究中的应用及研究进展，以期为RIHD的研究提供可靠的理论依据。

关键词: 放射性心脏病, 细胞模型, 标准化, 药物筛选

Abstract:

Radiation-induced heart disease is the most common and severe complication of radiation therapy for thoracic tumours. After exposure to radiation, cardiac tissue undergoes myocardial inflammation, fibrosis, and vascular endothelial damage, leading to cardiac dysfunction. With the continuous improvement of medical technology, the survival period of tumour patients has been significantly extended. However, RIHD severely impacts patients' quality of life. To thoroughly investigate its pathological mechanisms, establishing a reliable RIHD cell model is a crucial experimental foundation for studying its molecular mechanisms and evaluating treatment efficacy. This article reviews and summarises the application and research progress of RIHD cell models in related studies both domestically and internationally in recent years, aiming to provide a reliable theoretical basis for RIHD research.

Key words: radiation-induced, cellular model, standardization, drug screening

中图分类号:

R541
R730.55

王夏颖, 蒋虎刚, 任春贞, 马静, 刘佳坤, 刘凯, 李应东, 赵信科. 放射性心脏病体外模型的构建策略与应用挑战[J]. 中国临床药理学与治疗学, 2026, 31(5): 639-648.

Xiaying WANG, Hugang JIANG, Chunzhen REN, Jing MA, Jiakun LIU, Kai LIU, Yingdong LI, Xinke ZHAO. Construction strategy and application of an in vitro model of radioactive cardiac injury[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2026, 31(5): 639-648.

图/表 6

参考文献 66

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Detection target	Molecular biomarkers/functional indicators	Detection techniques	References
Oxidative stress	ROS levels, SOD activity, MDA content	DCFH-DA fluorescent probe	[6]
Apoptosis/vecrosis	Caspase-3 activity, Bax/Bcl-2 ratio, LDH release	Annexin V/PI double staining, Western Blot, LDH assay kit	[7]
Cell viability and proliferation	Cell survival rate, proliferation curve staining	CCK-8/MTT assay, EdU staining	[8]
DNA damage	γ-H2AX foci, ATM/ATR phosphorylation	Immunofluorescence, Western Blot	[9]
Fibrosis	TGF-β1, α-SMA, CollagenⅠ/Ⅲ	ELISA, Immunofluorescence, Sirius red staining	[10]
Mitochondrial dysfunction	ATP content, membrane potential (ΔΨm), mtROS	JC-1 probe (Flow cytometry), Seahorse XF Analyzer (oxygen consumption rate)	[24]
Inflammatory response	IL-6, TNF-α, IL-1β	(Luminex), RT-qPCR Multiplex liquid chip (Luminex), RT-qPCR (mRNA level)	[28]

Detection target	Molecular biomarkers/functional indicators	Detection techniques	References
Oxidative stress	ROS levels, SOD activity, MDA content	DCFH-DA fluorescent probe	[6]
Apoptosis/vecrosis	Caspase-3 activity, Bax/Bcl-2 ratio, LDH release	Annexin V/PI double staining, Western Blot, LDH assay kit	[7]
Cell viability and proliferation	Cell survival rate, proliferation curve staining	CCK-8/MTT assay, EdU staining	[8]
DNA damage	γ-H2AX foci, ATM/ATR phosphorylation	Immunofluorescence, Western Blot	[9]
Fibrosis	TGF-β1, α-SMA, CollagenⅠ/Ⅲ	ELISA, Immunofluorescence, Sirius red staining	[10]
Mitochondrial dysfunction	ATP content, membrane potential (ΔΨm), mtROS	JC-1 probe (Flow cytometry), Seahorse XF Analyzer (oxygen consumption rate)	[24]
Inflammatory response	IL-6, TNF-α, IL-1β	(Luminex), RT-qPCR Multiplex liquid chip (Luminex), RT-qPCR (mRNA level)	[28]

Drugs	Cell model	Dosage	Time	Method	Mechanisms	Therapeutic effects	References
Angelica-hedysarum polysaccharide	H9C2 irradiated with 2 Gy X-ray, detected at 24 h	400 mg/L	24 h	DEME	Rho/Rock↓	Anti-fibrotic, inhibits myocardial remodeling	[51]
Astragalus injection	CFs irradiated with 2 Gy X-ray, detected at 48 h	10 μg/mL 20 μg/mL	48 h	DEME	TGF-β1↓ Col-Ⅰ↓	Reduces ROS, inhibits ER stress and fibrosis	[7]
Shenmai injection	H9C2 irradiated with 20 Gy X-ray, detected at 72 h	1 μL/mL 5 μL/mL	72 h	DEME	ROS↓	Inhibits myocardial fibrosis and macrophage infiltration	[62]
Salidroside	H9C2 irradiated with 6 Gy X-ray, detected at 48 h	0.50 mmol/L	24 h	DEME	Bcl-2/Bax↑	Anti-inflammatory; mitigates cardiac injury	[50]
Angelica- hedysarum ultrafiltrate	H9C2 irradiated with 6 Gy X-ray, detected at 24 h	3,6,9 mg/mL	48 h	DEME	LDH↓, Bax, SOD↑	Antioxidant; reduces myocardial cell damage	[61]
Resveratrol	H9C2 irradiated with 4 Gy X-ray, detected at 48 h	50 μmol/L	24 h	DEME	TGF-β1↓	Alleviates oxidative stress and inflammation	[63]
Astragalus polysaccharide	H9C2 irradiated with 4 Gy X-ray, detected at 24 h	400 μg/mL	48 h	DEME	PI3K/Akt/ mTOR↑	Improves radiation-induced autophagic flux; reduces apoptosis and atrophy	[52]
Astragalosides	CFs irradiated with 1 Gy X-ray, detected at 48 h	20 mg/mL	48 h	DEME	TGF-β1 Col-Ⅰ↓	Reduces ROS; alleviates radiation-induced fibrosis	[64]
Astragaloside IV	HUVECs irradiated with 4 Gy X-ray, detected at 24 h	100 μg/mL	12 h	DEME	SOD↑	Anti-inflammatory; mitigates cardiac injury	[65]

Drugs	Cell model	Dosage	Time	Method	Mechanisms	Therapeutic effects	References
Angelica-hedysarum polysaccharide	H9C2 irradiated with 2 Gy X-ray, detected at 24 h	400 mg/L	24 h	DEME	Rho/Rock↓	Anti-fibrotic, inhibits myocardial remodeling	[51]
Astragalus injection	CFs irradiated with 2 Gy X-ray, detected at 48 h	10 μg/mL 20 μg/mL	48 h	DEME	TGF-β1↓ Col-Ⅰ↓	Reduces ROS, inhibits ER stress and fibrosis	[7]
Shenmai injection	H9C2 irradiated with 20 Gy X-ray, detected at 72 h	1 μL/mL 5 μL/mL	72 h	DEME	ROS↓	Inhibits myocardial fibrosis and macrophage infiltration	[62]
Salidroside	H9C2 irradiated with 6 Gy X-ray, detected at 48 h	0.50 mmol/L	24 h	DEME	Bcl-2/Bax↑	Anti-inflammatory; mitigates cardiac injury	[50]
Angelica- hedysarum ultrafiltrate	H9C2 irradiated with 6 Gy X-ray, detected at 24 h	3,6,9 mg/mL	48 h	DEME	LDH↓, Bax, SOD↑	Antioxidant; reduces myocardial cell damage	[61]
Resveratrol	H9C2 irradiated with 4 Gy X-ray, detected at 48 h	50 μmol/L	24 h	DEME	TGF-β1↓	Alleviates oxidative stress and inflammation	[63]
Astragalus polysaccharide	H9C2 irradiated with 4 Gy X-ray, detected at 24 h	400 μg/mL	48 h	DEME	PI3K/Akt/ mTOR↑	Improves radiation-induced autophagic flux; reduces apoptosis and atrophy	[52]
Astragalosides	CFs irradiated with 1 Gy X-ray, detected at 48 h	20 mg/mL	48 h	DEME	TGF-β1 Col-Ⅰ↓	Reduces ROS; alleviates radiation-induced fibrosis	[64]
Astragaloside IV	HUVECs irradiated with 4 Gy X-ray, detected at 24 h	100 μg/mL	12 h	DEME	SOD↑	Anti-inflammatory; mitigates cardiac injury	[65]

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放射性心脏病体外模型的构建策略与应用挑战

Construction strategy and application of an in vitro model of radioactive cardiac injury

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