阿霉素（Dox）被广泛用作抗肿瘤药物，但其严重的心脏毒性极大地限制了其临床应用。目前针对阿霉素引起的心脏毒性的治疗方法还不够，需要替代解决方案。本研究评估了垂盆草素（一种来自垂盆草的化合物）对阿霉素诱导的心脏毒性和功能障碍的影响。在暴露于 Dox 之前，对小鼠和 H9c2 细胞施用 Sarmentosin 作为预处理。随后，测量了血清和细胞上清液中阿霉素诱导的心脏毒性和铁死亡的标记物。利用蛋白质印迹分析来检测铁死亡、氧化应激和自噬蛋白的水平。此外，还采用超声心动图、苏木精-伊红染色、ROS 检测和免疫荧光技术来支持我们的发现。结果表明，垂柳菌素显着抑制铁积累、脂质过氧化和氧化应激，从而减少 Dox 诱导的 C57BL/6 小鼠和 H9c2 细胞的铁死亡和心脏毒性。其机制涉及自噬的激活和Nrf2信号通路。这些发现表明，莎门妥菌素可以通过减轻铁死亡来预防阿霉素诱导的心脏毒性。该研究强调了像莎曼妥辛这样的化合物在治疗阿霉素引起的心脏毒性方面的潜力。

Doxorubicin (Dox) is extensively used as an antitumor agent, but its severe cardiotoxicity significantly limits its clinical use. Current treatments for Dox-induced cardiotoxicity are inadequate, necessitating alternative solutions. This study evaluated the effects of sarmentosin, a compound from Sedum sarmentosum, on Dox-induced cardiotoxicity and dysfunction. Sarmentosin was administered as a pretreatment to both mice and H9c2 cells before Dox exposure. Subsequently, markers of Dox-induced cardiotoxicity and ferroptosis in serum and cell supernatants were measured. Western blot analysis was utilized to detect levels of ferroptosis, oxidative stress, and autophagy proteins. Additionally, echocardiography, hematoxylin-eosin staining, ROS detection, and immunofluorescence techniques were employed to support our findings. Results demonstrated that sarmentosin significantly inhibited iron accumulation, lipid peroxidation, and oxidative stress, thereby reducing Dox-induced ferroptosis and cardiotoxicity in C57BL/6 mice and H9c2 cells. The mechanism involved the activation of autophagy and the Nrf2 signaling pathway. These findings suggest that sarmentosin may prevent Dox-induced cardiotoxicity by mitigating ferroptosis. The study underscores the potential of compounds like sarmentosin in treating Dox-induced cardiotoxicity.