Department of Pediatrics, Chonbuk National University Hospital, 634-18 Keumam-dong, Jeonju 561-712, Republic of Korea.
J Nat Med. 2012 Jan;66(1):149-57. doi: 10.1007/s11418-011-0567-1. Epub 2011 Aug 21.
Adriamycin (ADR) is a potent anticancer drug. Its clinical applications are limited due to its cardiotoxicity. Oxidative stress is responsible for cardiomyopathy induced by ADR. Previous studies have demonstrated that davallialactone (DAVA), extracted from mushroom Inonotus xeranticus, has potential antiplatelet aggregation activity and free radical scavenging properties. In this study, we investigated whether DAVA has protective effects against ADR-induced free radical accumulation and apoptosis in cardiac muscle cells and compared the effects of DAVA with N-acetylcysteine, a potent antioxidant. We evaluated the effect of DAVA on ADR-induced cytotoxicity by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and crystal violet staining, the reactive oxygen species (ROS) production by flow cytometry, and the expression of stress-related proteins like Cu/Zn superoxide dismutase (SOD), Mn-SOD, and the involvement of mitogen-activated protein kinase pathway by Western blot analysis. Apoptosis was assessed by nuclear condensation and the expression levels of pro-apoptotic proteins, such as caspase-3 and polyadenosine diphosphate-ribose polymerase (PARP). The cardio-protective effects of DAVA were also evaluated in an in vivo study in an animal model of ADR-induced acute cardiomyopathy. Our results showed that DAVA significantly increased the viability of doxorubicin-injured H9c2 cells and inhibited ADR-induced ROS production, apoptosis, and the expression of Cu/Zn SOD and Mn-SOD. DAVA also inhibited the expression of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK), which was activated by ADR. In the in vivo animal model, treatment involving DAVA significantly reduced cardiomyocyte lesions. These results suggest that DAVA is a potentially protective agent for ADR-induced cardiotoxicity in cardiomyocytes and can be a potential candidate to protect against cardiotoxicity in ADR-treated cancer patients.
阿霉素(ADR)是一种有效的抗癌药物。由于其心脏毒性,其临床应用受到限制。氧化应激是阿霉素引起心肌病的原因。先前的研究表明,从药用真菌云芝中提取的裂环烯醚萜内酯(DAVA)具有潜在的抗血小板聚集活性和自由基清除特性。在这项研究中,我们研究了 DAVA 是否对 ADR 诱导的心肌细胞自由基积累和细胞凋亡具有保护作用,并将 DAVA 的作用与具有强大抗氧化作用的 N-乙酰半胱氨酸进行了比较。我们通过 MTT(3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐)测定和结晶紫染色、流式细胞术检测活性氧(ROS)产生以及 Western blot 分析评估了 DAVA 对 ADR 诱导的细胞毒性的影响,检测了应激相关蛋白如铜/锌超氧化物歧化酶(Cu/Zn SOD)、Mn-SOD 的表达以及丝裂原活化蛋白激酶(MAPK)通路的参与。通过核固缩和促凋亡蛋白如半胱天冬酶-3 和多聚腺苷二磷酸核糖聚合酶(PARP)的表达水平评估细胞凋亡。还在阿霉素诱导的急性心肌病动物模型中进行了体内研究,评估了 DAVA 的心脏保护作用。结果表明,DAVA 可显著提高阿霉素损伤的 H9c2 细胞活力,抑制 ADR 诱导的 ROS 产生、凋亡以及 Cu/Zn SOD 和 Mn-SOD 的表达。DAVA 还抑制了细胞外信号调节激酶(ERK)和 c-Jun N 端激酶(JNK)的表达,而这两种激酶被 ADR 激活。在体内动物模型中,DAVA 的治疗可显著减少心肌细胞损伤。这些结果表明,DAVA 可能是一种保护阿霉素诱导的心肌细胞毒性的潜在药物,可作为预防阿霉素治疗的癌症患者心脏毒性的潜在候选药物。