Key result
Salvianolic acid B attenuates cisplatin-induced cardiac dysfunction and oxidative stress in mice via Nrf2 signaling.
Why the study?
The effect of Salvianolic acid B on cardiac damage caused by conventional cancer chemotherapy with cisplatin remains unclear.
Does Salvianolic acid B attenuate cisplatin-induced cardiac injury and oxidative stress in preclinical models?
Does Salvianolic acid B attenuate cisplatin-induced cardiac injury and oxidative stress in preclinical models?
Salvianolic acid B shows potential in mitigating cisplatin-induced cardiotoxicity by reducing apoptosis and oxidative stress via the Nrf2 pathway in preclinical models.
Cardiovascular complications have been well documented as the downside to conventional cancer chemotherapy. As a notable side effect of cisplatin (CDDP), cardiotoxicity represents a major obstacle to the successful treatment of cancer. It has been reported that Salvianolic acid B (SalB) possesses cardioprotective quality. However, the effect of SalB on cardiac damage caused by conventional cancer chemotherapy remains unclear. In this study, we clarified the protective effect of SalB on cisplatin-induced heart injury. Furthermore, in H9c2 cells, SalB dramatically reduced cisplatin-induced apoptosis and oxidative stress by modulating the nuclear factor erythroid-2-related factor 2 (Nrf2) signaling pathway. In conclusion, SalB had great potential in mitigating cisplatin-induced cardiac injury. Furthermore, more attention should be placed on natural active compounds containing SalB with antioxidant effects for the treatment of cardiomyopathy.
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Lin et al. (2021) studied Cisplatin-induced cardiac injury (n=36). Salvianolic acid B vs. Cisplatin alone was evaluated on Cardiac injury, dysfunction, and oxidative stress. Salvianolic acid B significantly attenuated cisplatin-induced cardiac dysfunction, cardiomyocyte apoptosis, and oxidative stress in mice and H9c2 cells by modulating the Nrf2 signaling pathway.
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