Cardioprotective potentials of myricetin on doxorubicin-induced cardiotoxicity based on biochemical and transcriptomic analysis
文献类型： 外文期刊
作者： Li, Jaili 1 ; Luo, Ting 1 ; Zhao, Yao 3 ; Wang, Dou 1 ; Jin, Yuanxiang 3 ; Wu, Zufang 1 ; Yang, Guiling 1 ; Qi, Xingjiang 3 ;
作者机构： 1.Ningbo Univ, State Key Lab Managing Biot & Chem Threats Qual &, Ningbo 315832, Zhejiang, Peoples R China
2.Zhejiang Acad Agr Sci, Inst Agroprod Safety & Nutr, State Key Lab Managing Biot & Chem Threats Qual &, Lab Hangzhou Risk Assessment Agr Prod,Minist Agr, Hangzhou 310021, Zhejiang, Peoples R China
3.Xianghu Lab, Hangzhou 311231, Zhejiang, Peoples R China
4.Zhejiang Univ Technol, Coll Biotechnol & Bioengn, Hangzhou 310032, Zhejiang, Peoples R China
5.Minist Agr & Rural Affairs, Key Lab Traceabil Agr Genet Modified Organisms, Beijing, Peoples R China
关键词： Myricetin; Doxorubicin-induced cardiotoxicity; Cardioprotective effects; Energy metabolism; AMPK pathway
期刊名称：BIOMEDICINE & PHARMACOTHERAPY （ 影响因子：6.9； 五年影响因子：6.8 ）
ISSN： 0753-3322
年卷期： 2024 年 175 卷
页码：
收录情况： SCI
摘要： Doxorubicin (DOX) is a commonly used anthracycline in cancer chemotherapy. The clinical application of DOX is constrained by its cardiotoxicity. Myricetin (MYR) is a natural flavonoid widely present in many plants with antioxidant and anti-inflammatory properties. However, MYR's beneficial effects and mechanisms in alleviating DOX-induced cardiotoxicity (DIC) remain unknown. C57BL/6 mice were injected with 15 mg/kg of DOX to establish the DIC, and MYR solutions were administrated by gavage to investigate its cardioprotective potentials. Histopathological analysis, physiological indicators assessment, transcriptomics analysis, and RT-qPCR were used to elucidate the potential mechanism of MYR in DIC treatment. MYR reduced cardiac injury produced by DOX, decreased levels of cTnI, AST, LDH, and BNP, and improved myocardial injury and fibrosis. MYR effectively prevented DOX-induced oxidative stress, such as lowered MDA levels and elevated SOD, CAT, and GSH activities. MYR effectively suppressed NLRP3 and ASC gene expression levels to inhibit pyroptosis while regulating Caspase1 and Bax levels to reduce cardiac cell apoptosis. According to the transcriptomic analysis, glucose and fatty acid metabolism were associated with differential gene expression. KEGG pathway analysis revealed differential gene enrichment in PPAR and AMPK pathways, among others. Following validation, MYR was found to alleviate DIC by regulating glycolipid metabolism and AMPK pathway-related genes. Our findings demonstrated that MYR could mitigate DIC by regulating the processes of oxidative stress, apoptosis, and pyroptosis. MYR is critical in
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