2023
DOI: 10.1039/d2fo03416f
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Daidzein ameliorates doxorubicin-induced cardiac injury by inhibiting autophagy and apoptosis in rats

Abstract: Backgrounds: Doxorubicin (Dox) is a classical antitumor antibiotic widely restricted for use due to its cardiotoxicity. Daidzein (Daid) is a soy isoflavone that enhances antioxidant enzyme systems and inhibits apoptosis...

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Cited by 14 publications
(11 citation statements)
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“…Doxorubicin (Dox) is commonly employed in the treatment of malignant tumors; however, its clinical use is significantly limited due to the occurrence of acute, sub-acute, or chronic side effects (Rivankar, 2014). Notably, Dox exhibits a high affinity for cardiomyocytes, thereby leading to cardiotoxicity (Wu et al, 2023). The availability of medications for the treatment or prevention of cardiotoxicity is limited.…”
Section: Discussionmentioning
confidence: 99%
“…Doxorubicin (Dox) is commonly employed in the treatment of malignant tumors; however, its clinical use is significantly limited due to the occurrence of acute, sub-acute, or chronic side effects (Rivankar, 2014). Notably, Dox exhibits a high affinity for cardiomyocytes, thereby leading to cardiotoxicity (Wu et al, 2023). The availability of medications for the treatment or prevention of cardiotoxicity is limited.…”
Section: Discussionmentioning
confidence: 99%
“…However, excessive autophagy could lead to non-apoptotic cell death. 63 Previous studies have demonstrated that autophagy is highly associated with MPTP-induced parkinsonism in zebrafish models. 28,29 On the one hand, autophagy activation can reduce oxidative stress and prevent neuronal degeneration, and on the other hand, excessive autophagy can promote apoptosis and lead to the occurrence of PD.…”
Section: Papermentioning
confidence: 99%
“…Daidzein is a soy isoflavone that has shown protective effects against doxorubicin-induced cardiac injury in rats, as pretreatment with a low quantity significantly improved cardiac function and relieved histopathological deterioration of cardiomyocytes alleviated by doxorubicin. It decreased the protein expression of LC3 II, Bax, p-Akt, and cleaved caspase3, while enhancing cyclin D1 and Bcl-2, decreased apoptosis and autophagy by downregulating the PI3K/Akt pathway, thus defending the hearts from doxorubicin-induced cardiac damage [ 111 ].…”
Section: Autophagymentioning
confidence: 99%