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作 者:王晓平 凌观静 李伟利 王伟 王勇[1,2,3] WANG XiaoPing;LING GuanJing;LI WeiLi;WANG Wei;WANG Yong(College of Chinese Medicine,Beijing University of Chinese Medicine,Beijing 100029,China;Beijing Key Laboratory of TCM Syndrome and Formula,Beijing 100029,China;Ministry of Education Key Laboratory of TCM Syndrome and Formula,Beijing 100029,China)
机构地区:[1]北京中医药大学中医学院,北京100029 [2]证候与方剂基础研究北京市重点实验室,北京100029 [3]证候与方剂基础研究教育部重点实验室,北京100029
出 处:《中国科学:生命科学》2022年第6期935-942,共8页Scientia Sinica(Vitae)
基 金:国家自然科学基金(批准号:81822049,82174364,81930113);科技部重大新药创制项目(批准号:2019ZX09201004-001-011)资助。
摘 要:蒽环类化疗药阿霉素(doxorubicin, DOX)是治疗各种癌症最有效的药物之一,然而其治疗效应受到相关心脏毒性的严重限制.尽管该领域研究众多,但DOX诱导心脏毒性(DOX-induced cardiotoxicity, DIC)的确切分子机制仍然值得进一步研究. DOX是一种线粒体毒素,线粒体损伤是DIC的核心.本文回顾大量文献并收集与DIC相关的依赖于线粒体功能障碍的机制,包括DOX对线粒体电子传递链、氧化还原循环、氧化应激、钙失调、细胞凋亡途径和线粒体自噬等的影响.此外,本文讨论了基于线粒体功能的中药预防和/或减轻DIC的现有策略,以期为DOX与中药的临床联合用药提供科学依据.Doxorubicin(DOX), an anthracycline chemotherapeutic drug, is one of the most effective drugs for the treatment of various cancers.However, its therapeutic effect is seriously limited by related cardiotoxicity. Although this field has yielded many studies, the exact molecular mechanism of DOX-induced cardiotoxicity(DIC) is still worthy of further study. DOX is a mitochondrial toxin, and mitochondrial damage is the core of DIC. This paper reviews a large amount of literature and summarizes the mechanisms related to DIC that depend on mitochondrial dysfunction, including the effects of DOX on mitochondrial electron transport chain, redox cycle,oxidative stress, calcium imbalance, apoptosis pathway and mitophagy. In addition, it discusses the existing strategies of traditional Chinese medicine based on mitochondrial function to prevent and/or reduce DIC, to provide a scientific basis for combination of DOX and traditional Chinese medicine in the treatment of cancer.
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