Key result
Amentoflavone protects mice from doxorubicin-induced cardiotoxicity by alleviating structural alterations and lowering CK-MB and AST.
Why the study?
Doxorubicin is an effective chemotherapeutic agent whose use is limited by cardiotoxicity, prompting investigation into whether amentoflavone can provide cardioprotection.
Does Amentoflavone prevent doxorubicin-induced cardiotoxicity in mice?
Does Amentoflavone prevent doxorubicin-induced cardiotoxicity in mice?
Amentoflavone shows potential as a cardioprotective agent against doxorubicin-induced cardiotoxicity in a mouse model via antioxidant, anti-inflammatory, and anti-apoptotic mechanisms.
Amentoflavone may mitigate doxorubicin cardiotoxicity in mice; leaves open translation to human cardioprotection.
Doxorubicin (DOX) is an available chemotherapeutic drug for treating various tumors. However, its effectiveness is limited by cardiotoxicity. Amentoflavone (AMF), a natural biflavonoid separated from Cycas thouarsii ethyl acetate fraction, displays promising anticancer, anti-inflammatory, and antioxidant effects. Thus, our research aims to explore whether AMF could boost cardioprotective effects against DOX cardiotoxicity and reveal the potential underlying mechanisms of cardioprotection. Mice were classified into four groups; Normal control, Untreated DOX group, and DOX groups treated with AMF (40 and 80 mg/kg, respectively) intraperitoneal injection daily for four days before doxorubicin administration and for additional three days following DOX administration to assess cardiotoxicity. Echocardiography showed that AMF 80 treated group was protected from DOX cardiotoxicity. Additionally, it alleviated histopathological structural alterations and effectively restored heart weight and body weight ratio. These effects were confirmed biochemically by a substantially reduced serum creatine kinase-MB (CK-MB) and aspartate aminotransferase (AST) levels. AMF effectively restored nuclear respiratory factor-1(NRF-1), mitochondrial transcription factor A (TFAM), and normalized heat shock protein - 27(HSP-27) expression levels compared to the DOX group. Moreover, AMF mitigated oxidative stress conditions and significantly suppressed NADPH oxidase (NOX) expression levels. It also showed significant anti-inflammatory effects via suppressing interleukin-6 (IL-6) expression and decreasing nuclear factor Kabba B (NF-κb) immune-staining. In addition, AMF markedly reduced FAS ligand (FASL) expression and p53 immune staining in cardiac tissue. This study is the first for the in vivo potential beneficial effects of AMF against acute DOX cardiotoxicity, possibly via exerting antioxidant, anti-inflammatory, and anti-apoptotic effects and restoring mitochondrial function.
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Alherz et al. (2022) studied Doxorubicin-induced cardiotoxicity. Amentoflavone vs. Untreated DOX group was evaluated on Cardiotoxicity. Amentoflavone at 80 mg/kg protected mice from doxorubicin-induced cardiotoxicity, alleviating structural alterations and reducing serum CK-MB and AST levels.
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