The current study evaluated the cardioprotective activity of genistein in cases of doxorubicin-(Dox) induced cardiac toxicity and a probable mechanism underlying this protection, such as an antioxidant pathway in cardiac tissues. Animals used in this study were categorized into four groups. The first group was treated with sodium carboxymethylcellulose (0.3%; CMC-Na) solution. The second group received Dox (3.0 mg/kg, i.p.) on days 6, 12, 18, and 24. The third and fourth groups received Dox (3 mg/kg, i.p.) on days 6, 12, 18, and 24 and received protective doses of genistein (100 [group 3] and 200 [group 4] mg/kg/day, p.o.) for 30 days. Treatment with genistein significantly improved the altered cardiac function markers and oxidative stress markers. This was coupled with significant improvement in cardiac histopathological features. Genistein enhanced the Nrf2 and HO-1 expression, which showed protection against oxidative insult induced by Dox. Terminal deoxynucleotidyl transferase dUTP nick end labeling assay showed substantial inhibition of apoptosis by genistein in myocardia. The study showed that genistein has a strong reactive oxygen species scavenging property and potentially (P ≤ .001) decreases the lipid peroxidation as well as inhibits DNA damage in cardiac toxicity induced by Dox. In conclusion, the potential antioxidant effect of genistein may be because of its modulatory effect on Nrf2/HO-1 signalling pathway and by this means exhibits cardioprotective effects from Dox-induced oxidative injury.

中文翻译：

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Nrf2 / HO-1介导染料木黄酮对阿霉素诱导的心脏毒性的保护作用。

目前的研究评估了染料木黄酮在阿霉素（Dox）引起的心脏毒性情况下的心脏保护活性以及这种保护作用的可能机制，例如心脏组织中的抗氧化剂途径。在这项研究中使用的动物分为四组。第一组用羧甲基纤维素钠（0.3％； CMC-Na）溶液处理。第二组在第6、12、18和24天接受Dox（3.0 mg / kg，ip）。第三和第四组在第6、12、18和24天接受Dox（3 mg / kg，ip）。接受了30天内保护剂量的染料木黄酮（100 [组3]和200 [组4] mg / kg /天，口服）。金雀异黄素的治疗显着改善了改变的心脏功能标志物和氧化应激标志物。这与心脏组织病理学特征的显着改善相结合。金雀异黄素增强了Nrf2和HO-1的表达，显示出对Dox诱导的氧化损伤的保护作用。末端脱氧核苷酸转移酶dUTP缺口末端标记检测显示，染料木黄酮可抑制心肌细胞凋亡。研究表明，染料木黄酮具有很强的清除活性氧的特性，并且可能（P≤.001）降低脂质过氧化作用，并抑制Dox引起的心脏毒性中的DNA损伤。总之，金雀异黄素潜在的抗氧化作用可能是由于其对Nrf2 / HO-1信号通路的调节作用，并因此表现出Dox诱导的氧化损伤的心脏保护作用。末端脱氧核苷酸转移酶dUTP缺口末端标记检测显示，染料木黄酮可抑制心肌细胞凋亡。研究表明，染料木黄酮具有很强的清除活性氧的特性，并且可能（P≤.001）降低脂质过氧化作用，并抑制Dox引起的心脏毒性中的DNA损伤。总之，金雀异黄素潜在的抗氧化作用可能是由于其对Nrf2 / HO-1信号通路的调节作用，并因此表现出Dox诱导的氧化损伤的心脏保护作用。末端脱氧核苷酸转移酶dUTP缺口末端标记检测显示，染料木黄酮可抑制心肌细胞凋亡。研究表明，染料木黄酮具有很强的清除活性氧的特性，并且可能（P≤.001）降低脂质过氧化作用，并抑制Dox引起的心脏毒性中的DNA损伤。总之，金雀异黄素潜在的抗氧化作用可能是由于其对Nrf2 / HO-1信号通路的调节作用，并因此表现出Dox诱导的氧化损伤的心脏保护作用。