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首页|期刊导航|中国药理学通报|丹参酮ⅡA在放射性心脏损伤防治中的作用机制及研究进展

丹参酮ⅡA在放射性心脏损伤防治中的作用机制及研究进展

李燕玲 高志凌 王刚 谢萍

中国药理学通报2025,Vol.41Issue(12):2236-2240,5.
中国药理学通报2025,Vol.41Issue(12):2236-2240,5.DOI:10.12360/CPB202503099

丹参酮ⅡA在放射性心脏损伤防治中的作用机制及研究进展

Mechanisms and research progress of tanshinone ⅡA in the prevention and treatment of radiation-induced heart disease

李燕玲 1高志凌 2王刚 2谢萍1

作者信息

  • 1. 甘肃中医药大学中西医结合学院||甘肃省人民医院心血管内科一病区,甘肃兰州 730000
  • 2. 甘肃省人民医院心血管内科一病区,甘肃兰州 730000
  • 折叠

摘要

Abstract

Radiation-induced heart disease(RIHD)is a common and severe complication following radiotherapy for thoracic tumors,significantly impacting patients' long-term prognosis and quality of life.Its pathogenesis is complex,primarily involving oxidative stress,inflammatory responses,endothelial dysfunction,and chronic fibrosis.Currently,there is a lack of effective clini-cal prevention and treatment methods,highlighting the urgent need to develop intervention strategies for RIHD.Tanshinone ⅡA,the main active component of Salvia miltiorrhiza,exhibits mul-tiple pharmacological effects,including antioxidant,anti-inflam-matory,anti-fibrotic,and anti-apoptotic properties.Studies have shown that Tanshinone ⅡA can significantly mitigate radiation-induced myocardial injury and fibrosis,as well as improve cardi-ac function,by scavenging reactive oxygen species,inhibiting in-flammatory pathways,and modulating fibrotic signaling path-ways.This article summarizes the pathogenesis of RIHD and the research progress on Tanshinone ⅡA in the prevention and treat-ment of RIHD,providing new theoretical insights for developing effective cardioprotective strategies.

关键词

放射性心脏损伤/丹参酮ⅡA/作用机制/氧化应激/纤维化/靶点/治疗

Key words

Radiation-induced heart disease/Tanshinone ⅡA/Mechanism of action/Oxidative stress/Fibrosis/Target/Thera-py

分类

医药卫生

引用本文复制引用

李燕玲,高志凌,王刚,谢萍..丹参酮ⅡA在放射性心脏损伤防治中的作用机制及研究进展[J].中国药理学通报,2025,41(12):2236-2240,5.

基金项目

国家自然科学基金资助项目(No 82460051) (No 82460051)

甘肃省自然科学基金资助项目(No 25JRRA286) (No 25JRRA286)

甘肃省人民医院院内基金资助项目(No 24GSSYE-15) (No 24GSSYE-15)

中国药理学通报

OA北大核心

1001-1978

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