Project description:Doxorubicin (DOXO), a chemotherapeutic drug, is cardiotoxic. We hypothesized that folic acid is an effective therapeutic agent in a mouse model of DOXO-induced cardiotoxicity. We performed genome-wide expression profiling to identify the underlying mechanisms.
Project description:Doxorubicin (DOXO), a chemotherapeutic drug, is cardiotoxic. We hypothesized that folic acid is an effective therapeutic agent in a mouse model of DOXO-induced cardiotoxicity. We performed genome-wide expression profiling to identify the underlying mechanisms. Male C57Bl6 2-mo old mice received DOXO (1x20 mg/kg, ip) or saline (sham). FA (10 mg/d) or placebo (plac) was administered 7d before DOXO administration until the end of the experiment (10d).
Project description:The FDA approved drug Doxorubicin provokes copious irreversible cardiotoxicity and even increases the risk of heart failure. Considering the multiple and interacted molecular pathways in cancer, there is a big possibility that tumors are simultaneously sensitive to different drugs. This makes achievable to study the combinations of drug, having the virtues of less toxicity, higher efficacy and potentially antagonizing drug resistance in cancer therapy. In the present study, we addressed the synergistic effects of ginsenoside Rh2 on doxorubicin-treated breast cancer bearing mice. We showed that Rh2 significantly enhanced the anti-cancer effects of doxorubicin and greatly attenuated the cardiotoxicity. Transcriptomic changes can clearly distinguish the chemotherapeutic groups and non-treated control groups. Transcriptomic analysis domestrated that Rh2 protection involved in multiple vital pathways including cellular stress, apoptosis and inflammation.
Project description:The FDA approved drug Doxorubicin provokes copious irreversible cardiotoxicity and even increases the risk of heart failure. Considering the multiple and interacted molecular pathways in cancer, there is a big possibility that tumors are simultaneously sensitive to different drugs. This makes achievable to study the combinations of drug, having the virtues of less toxicity, higher efficacy and potentially antagonizing drug resistance in cancer therapy. In the present study, we addressed the synergistic effects of ginsenoside Rh2 on doxorubicin-treated breast cancer bearing mice. We showed that Rh2 significantly enhanced the antitumor effects of doxorubicin and greatly attenuated the cardiotoxicity. Transcriptomic changes can clearly distinguish the chemotherapeutic groups and non-treated control groups. Transcriptomic analysis domestrated that Rh2 protection involved in multiple vital pathways including cellular senescece, fibrosis remodeling, apoptosis and inflammation.
