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Updated: Feb 4, 2026

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
Published on: May 16, 2020
Ganoderma atrum polysaccharide improves doxorubicin-induced cardiotoxicity in mice by regulation of apoptotic pathway
Wen-Juan Li1, Xian-Yi Zhang1, Rui-Ting Wu1
1State Key Laboratory of Food Science and Technology, Nanchang University, 235 Nanjing East Road, Nanchang 330047, China.
Abstract:
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.
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