Shabalala S, Muller C J F, Louw J, Johnson R
Biomedical Research and Innovation Platform, South African Medical Research Council, P.O. Box 19070, Tygerberg 7505, South Africa; Department of Biochemistry and Microbiology, University of Zululand, Kwa-Dlangezwa, 3886, South Africa.
Biomedical Research and Innovation Platform, South African Medical Research Council, P.O. Box 19070, Tygerberg 7505, South Africa; Department of Biochemistry and Microbiology, University of Zululand, Kwa-Dlangezwa, 3886, South Africa; Division of Medical Physiology, Faculty of Medicine and Health Sciences, Stellenbosch University, Tygerberg 7507, South Africa.
Life Sci. 2017 Jul 1;180:160-170. doi: 10.1016/j.lfs.2017.05.003. Epub 2017 May 3.
Doxorubicin is a highly effective, first line chemotherapeutic agent used in the management of hematological and solid tumors. The effective use of doxorubicin in cancer therapy has been severely limited owing to its well-documented cardiotoxic side effect. Oxidative stress, lipid peroxidation, apoptosis as well as dysregulation of autophagy, has been implicated as a major contributor associated with doxorubicin-induced cardiotoxicity. Increased oxidative stress and lipid peroxidation are known to enhance the production of reactive oxygen species, while autophagy has been reported to protect the cell from stress stimuli or, alternatively, contribute to cell death. Nonetheless, to date, no single chemical synthesized drug is available to prevent the harmful action of doxorubicin without reducing its anti-cancer efficacy. Therefore, the search for an effective and safe antagonist of doxorubicin-induced cardiotoxicity remains a challenge. In recent years, there has been much interest in the role plant-derived polyphenols play in the regulation of oxidative stress and autophagy. Therefore, the present review renders a concise overview of the mechanism associated with doxorubicin-induced cardiotoxicity as well as giving insight into the role plant-derived phytochemical play as a possible adjunctive therapy against the development of doxorubicin-induced cardiotoxicity.
阿霉素是一种高效的一线化疗药物,用于治疗血液系统肿瘤和实体瘤。由于其已被充分证明的心脏毒性副作用,阿霉素在癌症治疗中的有效应用受到了严重限制。氧化应激、脂质过氧化、细胞凋亡以及自噬失调,被认为是与阿霉素诱导的心脏毒性相关的主要因素。已知氧化应激和脂质过氧化增加会增强活性氧的产生,而据报道自噬可保护细胞免受应激刺激,或者导致细胞死亡。尽管如此,迄今为止,尚无单一的化学合成药物能够在不降低其抗癌疗效的情况下预防阿霉素的有害作用。因此,寻找一种有效且安全的阿霉素诱导心脏毒性拮抗剂仍然是一项挑战。近年来,植物源多酚在调节氧化应激和自噬中的作用备受关注。因此,本综述简要概述了与阿霉素诱导心脏毒性相关的机制,并深入探讨了植物源植物化学物质作为对抗阿霉素诱导心脏毒性发展的可能辅助治疗手段所起的作用。