Key result
Tetrandrine supplementation improved cardiac function and prevented the development of doxorubicin-related cardiac injury in mice through activation of Nrf2.
Why the study?
Whether tetrandrine could attenuate doxorubicin-related cardiotoxicity remained unclear.
Does tetrandrine prevent doxorubicin-induced acute cardiac injury in mice?
Does tetrandrine prevent doxorubicin-induced acute cardiac injury in mice?
Tetrandrine attenuates doxorubicin-induced acute cardiac injury in mice by reducing oxidative damage and apoptosis through the activation of Nrf2.
Answers are grounded in this paper and cite their sources.
Supports Nrf2 activation against doxorubicin cardiotoxicity in mice; leaves open translation to human cardioprotection.
Oxidative damage is closely involved in the development of doxorubicin- (DOX-) induced cardiotoxicity. It has been reported that tetrandrine can prevent the development of cardiac hypertrophy by suppressing reactive oxygen species- (ROS-) dependent signaling pathways in mice. However, whether tetrandrine could attenuate DOX-related cardiotoxicity remains unclear. To explore the protective effect of tetrandrine, mice were orally given a dose of tetrandrine (50 mg/kg) for 4 days beginning one day before DOX injection. To induce acute cardiac injury, the mice were exposed to a single intraperitoneal injection of DOX (15 mg/kg). The data in our study showed that tetrandrine prevented DOX-related whole-body wasting and heart atrophy, decreased markers of cardiac injury, and improved cardiac function in mice. Moreover, tetrandrine supplementation protected the mice against oxidative damage and myocardial apoptotic death. Tetrandrine supplementation also reduced ROS production and improved cell viability after DOX exposure in vitro. We also found that tetrandrine supplementation increased nuclear factor (erythroid-derived 2)-like 2 (Nrf2) expression and activity in vivo and in vitro. The protection of tetrandrine supplementation was blocked by Nrf2 deficiency in mice. In conclusion, our study found that tetrandrine could improve cardiac function and prevent the development of DOX-related cardiac injury through activation of Nrf2.
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Li et al. (2020) studied Doxorubicin-induced acute cardiac injury. Tetrandrine vs. Doxorubicin alone was evaluated on Cardiac injury, cardiac function, oxidative damage, and myocardial apoptotic death. Tetrandrine supplementation improved cardiac function and prevented the development of doxorubicin-related cardiac injury in mice through activation of Nrf2.
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