Selenium Attenuates Doxorubicin-Induced Cardiotoxicity Through Nrf2-NLRP3 Pathway

Selenium (Se), an essential nutrient for humans, has been reported to possess cardioprotective effect. However, the protective effects of Se against doxorubicin (DOX)-induced cardiotoxicity and the underlying mechanism are rarely reported. In this study, we sought to explore whether Se protected aga...

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Bibliographic Details
Published in:Biological trace element research 2022-06, Vol.200 (6), p.2848-2856
Main Authors: Yang, Hai-Bing, Lu, Zhao-Yang, Yuan, Wei, Li, Wei-Dong, Mao, Shang
Format: Article
Language:English
Subjects:
Biochemistry
Biomedical and Life Sciences
Biotechnology
Cardiotoxicity
Cytokines
Doxorubicin
Heart
Inflammasomes
Inflammation
Life Sciences
Nutrition
Oncology
Selenium
Supplements
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Summary:Selenium (Se), an essential nutrient for humans, has been reported to possess cardioprotective effect. However, the protective effects of Se against doxorubicin (DOX)-induced cardiotoxicity and the underlying mechanism are rarely reported. In this study, we sought to explore whether Se protected against DOX-induced cardiotoxicity by inhibiting Nrf2-NLRP3 pathway. We found that Se treatment effectively alleviated DOX-induced myocardial dysfunctions, decreasing plasma markers associated with myocardial injury. Moreover, Se treatment significantly inhibited DOX-induced oxidative damages and pro-inflammatory cytokine expression in heart tissues. Furthermore, Se treatment markedly promoted the expression of Nrf2 and prevented the activation of NLRP3 inflammasome. Importantly, suppression of Nrf2 abolished the cardioprotective effects of Se and diminished the inhibition of Se on NLRP3 inflammasome. Collectively, our study demonstrated that Se might protect against DOX-induced cardiotoxicity via regulating Nrf2-NLRP3 pathway. Se supplementation may be a potential therapeutic strategy to protect against DOX-induced cardiac injury.
ISSN:0163-4984
1559-0720
DOI:10.1007/s12011-021-02891-z