Clinically, the use of doxorubicin (DOX) is limited due to DOX-induced cardiotoxicity (DIC). The current study aimed to evaluate the cardioprotective effect of trehalose (TRE) against DIC in a female Swiss albino mouse model. Mice were divided into five experimental groups: Gp. I: saline control group (200 μl/mouse saline three times per week for 3 weeks day after day), Gp. II: DOX-treated group (2 mg/kg body weight three times per week for 3 weeks day after day), Gp. III: TRE group (200 μg/mouse three times per week for 3 weeks day after day), Gp. IV: DOX + TRE cotreatment group (animals were coadministered with DOX and TRE as in Gp. II and III, respectively), and Gp. V: DOX + TRE posttreatment group (animals were treated with DOX as in Gp. II followed by treatment with TRE as in Gp. III). DOX-treated mice showed significant elevation in cardiac injury biomarkers (lactate dehydrogenase, creatine kinase isoenzyme-MB, and cardiac troponin I), cardiac oxidative stress (OS) markers (malondialdehyde and myeloperoxidase), and cardiac levels of autophagy-related protein 5. Moreover, DOX significantly reduced the levels of total antioxidant capacity and activities of catalase and glutathione S-transferase. In contrast, TRE treatment of DOX-administered mice significantly improved almost all of the above-mentioned assessed parameters. Furthermore, histopathological changes of cardiac tissues observed in mice treated with TRE in combination with DOX were significantly improved as compared to DOX-treated animals. Taken together, the present study provides evidence that TRE has cardioprotective effects against DIC, which is likely mediated via suppression of OS and autophagy.

中文翻译：

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海藻糖通过抑制氧化应激和自噬减轻多柔比星诱导的雌性瑞士白化小鼠心脏毒性

临床上，由于 DOX 诱导的心脏毒性 (DIC)，阿霉素 (DOX) 的使用受到限制。目前的研究旨在评估海藻糖 (TRE) 在雌性瑞士白化小鼠模型中对 DIC 的心脏保护作用。小鼠被分成五个实验组：Gp。I：生理盐水对照组（200 μl/小鼠生理盐水，每周 3 次，连续 3 周，日复一日），Gp。II：DOX 治疗组（2mg/kg 体重，每周 3 次，连续 3 周，日复一日），Gp。III：TRE 组（200 μg/小鼠，每周 3 次，连续 3 周，日复一日），Gp。IV：DOX + TRE 共同治疗组（动物与 DOX 和 TRE 共同给药，分别在 Gp. II 和 III 中），和 Gp。V：DOX + TRE 后处理组（动物在 Gp. II 中用 DOX 处理，然后在 Gp. III 中用 TRE 处理）。DOX 治疗的小鼠心脏损伤生物标志物（乳酸脱氢酶、肌酸激酶同工酶-MB 和心肌肌钙蛋白 I）、心脏氧化应激 (OS) 标志物（丙二醛和髓过氧化物酶）和自噬相关蛋白 5 的心脏水平显着升高。此外，DOX 显着降低了总抗氧化能力和过氧化氢酶和谷胱甘肽 S-转移酶活性的水平。相比之下，DOX 给药小鼠的 TRE 治疗显着改善了几乎所有上述评估参数。此外，与 DOX 治疗的动物相比，在用 TRE 和 DOX 治疗的小鼠中观察到的心脏组织的组织病理学变化显着改善。总之，本研究提供的证据表明 TRE 对 DIC 具有心脏保护作用，