Key result
Biochanin A inhibits doxorubicin-induced cardiac dysfunction and fibrosis in mice while enhancing tumor suppression.
Why the study?
Doxorubicin-induced cardiotoxicity impacts cancer prognosis, and whether biochanin A can inhibit doxorubicin-induced myocardial injury without diminishing its anticancer efficacy is unclear.
Does Biochanin A alleviate doxorubicin-induced cardiotoxicity without interfering with its anti-tumor effect in tumor-bearing mice?
Does Biochanin A alleviate doxorubicin-induced cardiotoxicity without interfering with its anti-tumor effect in tumor-bearing mice?
Biochanin A alleviates doxorubicin-induced cardiotoxicity and cooperates with doxorubicin to inhibit tumor growth in preclinical models.
BACKGROUND AND AIM: Doxorubicin (DOX)-induced cardiotoxicity (DIC) by the chemotherapeutic drug seriously affects the prognosis of patients with cancer. Therefore, it is significant to actively explore the underlying mechanisms of DIC and develop safe and effective adjuvant therapies to improve DIC. As a traditional Chinese medicine monomer, BCA can treat cardiovascular diseases. However, whether BCA is able to inhibit DOX-induced myocardial injury without affecting its anticancer effect is unclear. EXPERIMENTAL PROCEDURE: We divided tumor-bearing mice into four groups, constructed a heart failure model by administering DOX, and treated with BCA. Histopathological staining was performed (WGA, HE, IF, IHC, etc.), WB, qPCR, and serum detection of SOD and MDA. In vitro experiments, the effects of BCA and DOX in both kinds of cells were demonstrated by various experiments in primary cardiomyocytes and tumor cells panc02 of neonatal rats. KEY RESULTS: The results showed that BCA could inhibit DOX-induced abnormal cardiac function in mice, improve heart failure, and inhibit the expression of ANP and BNP. It inhibited the level of myocardial oxidative stress and reduced the number of myocardial vacuolation and the degree of myocardial fibrosis in mice. BCA reduced DOX-induced oxidative stress in NRCMs. In terms of tumors, BCA cooperates with DOX to inhibit the occurrence and development of panc02 and reduce the body weight of tumors. It inhibited the expression of PCNA and promoted the expression of BAX. In vitro experiments, BCA cooperated with DOX to inhibit the proliferation and metastasis of panc02. CONCLUSIONS AND IMPLICATIONS: To sum up, BCA can affect the occurrence and development of DOX-induced myocardial injury through multiple targets and pathways and does not interfere with the anti-tumor effect of DOX. This study seeks new drugs for DOX-induced myocardial injury and provides new ideas for the treatment of inhibiting DOX-induced myocardial injury and the research of related diseases.
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Yang et al. (2025) studied Doxorubicin-induced cardiotoxicity. Biochanin A (BCA) vs. Doxorubicin alone / control was evaluated on Cardiac function, myocardial oxidative stress, and tumor growth. Biochanin A inhibited doxorubicin-induced abnormal cardiac function, myocardial oxidative stress, and fibrosis in mice, while cooperating with doxorubicin to inhibit tumor growth.
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