A novel therapeutic approach to doxorubicin-induced cardiotoxicity, with a particular emphasis on the potential cardioprotective properties of Vitis gracilis Wall.

Context: Doxorubicin, a potent chemotherapy drug, often leads to cardiotoxicity, limiting its clinical use. This study investigates the potential of Vitis gracilis Wall. nanoherbs (VGN) in mitigating doxorubicin-induced heart damage, aiming to provide insights into its therapeutic efficacy as a cardioprotective agent. Aims: To evaluate the therapeutic potential of VGN in mitigating doxorubicin-induced cardiotoxicity. Methods: The study comprised four treatment groups in male Wistar rats: D0 (negative control), D+ (doxorubicin 0.00038 mg/200 g body weight (BW)/day), DC (doxorubicin + Vitamin C 0.04 mg/200 g BW/d), D25 (doxorubicin + VGN at 25 mg/200 g BW/d), and D30 (doxorubicin + VGN at 30 mg/200 g BW/d). Key cardiac parameters, including LDH, CK-MB, TNF-alpha, IL-10, SOD, and caspase 3, were meticulously measured to assess cardioprotective effects. Statistical analyses were performed to evaluate the significance of observed changes, revealing a dose-dependent reduction in markers of cardiac injury (LDH, CK-MB) and inflammation (TNF-alpha) alongside enhancements in antioxidant defenses (SOD) and inhibition of apoptosis (caspase 3) with VGN administration. Results: The results showed promising reductions in markers of heart injury (LDH, CK-MB) and inflammation (TNF-alpha) specifically at a dose of 30 mg/200 g BW/d significantly (p<0.05). In addition, doses of 30 mg/200 g BW/d of VGN showed potential to increase antioxidant defenses (SOD), IL-10, as well as inhibit apoptosis (caspase 3) (p<0.05), highlighting the best multifaceted cardioprotective effects. Conclusions: The study demonstrates that V. gracilis has the potential to reduce doxorubicin-induced cardiotoxicity through its multifaceted cardioprotective effects. These effects include a reduction in markers of cardiac injury and inflammation at a dose of 30 mg/200 g BW/d, enhancement of antioxidant defenses, and inhibition of apoptosis.