心脏毒性
丙二醛
氧化应激
阿霉素
药理学
乳酸脱氢酶
谷胱甘肽
过氧化氢酶
医学
谷胱甘肽过氧化物酶
生理盐水
肾毒性
肌酸激酶
内分泌学
化学
内科学
毒性
化疗
生物化学
酶
作者
Rasha Abu-Khudir,Wafaa Ibrahim,Mohammed E. Shams,Afrah F. Salama
摘要
Abstract 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.
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