The present study aimed to determine the cardioprotective effect of Ganoderma atrum polysaccharide (PSG-1) in doxorubicin (DOX)-treated mice and its underlying mechanism. Results indicated that PSG-1 treatment significantly alleviated DOX-induced myocardial damage via attenuating apoptosis and maintaining the structure of myocardial mitochondria. Meanwhile, PSG-1-evoked cardioprotection was associated with an increase of manganese superoxide dismutase activity and decrease of caspases activities. Moreover, administration of PSG-1 suppressed DOX-induced mitochondrial disorders, which was evidenced by reducing reactive oxygen species, elevating mitochondrial membrane potential and inhibiting the opening of mitochondrial permeability transition pore. PSG-1 was also found to reduce the release of cytochrome c from mitochondria to cytoplasm in mice subjected to DOX. Finally, our findings have provided comprehensive evidence for the cardioprotective effects of PSG-1 via reduction of apoptosis mediated by modification of the mitochondrial intrinsic apoptotic pathway, indicating that PSG-1 could be developed as an effective therapeutic strategy to prevent DOX-induced cardiotoxicity in clinical settings.

本研究旨在确定灵芝atrum多糖（PSG-1）在阿霉素（DOX）处理的小鼠中的心脏保护作用及其潜在机制。结果表明，PSG-1治疗可通过减轻细胞凋亡并维持心肌线粒体的结构来显着减轻DOX诱导的心肌损伤。同时，PSG-1引起的心脏保护作用与锰超氧化物歧化酶活性的增加和胱天蛋白酶活性的降低有关。此外，施用PSG-1可抑制DOX诱导的线粒体疾病，这可通过减少活性氧，提高线粒体膜电位和抑制线粒体通透性转换孔的开放来证明。还发现PSG-1减少了接受DOX的小鼠中细胞色素c从线粒体到细胞质的释放。最后，我们的发现为通过减少线粒体固有凋亡途径介导的凋亡减少PSG-1的心脏保护作用提供了全面的证据，表明PSG-1可以作为预防DOX诱导的心脏毒性的有效治疗策略而开发。临床设置。