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Antioxidants
Volume 14
Issue 12
10.3390/antiox14121461
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Article

Cistanche deserticola Polysaccharides Protect Against Doxorubicin-Induced Cardiotoxicity via Antioxidant and Mitochondrial Mechanisms

by
Jingyi Qi
,
Yang Zhang
,
Mingyang Cui
,
Yufang Shi
,
Xinyu Luo
,
Chang Fan
,
Sitong Wan
,
Peng An
,
Yongting Luo
* and
Junjie Luo
*
Department of Nutrition and Health, China Agricultural University, Beijing 100193, China
*
Authors to whom correspondence should be addressed.
Antioxidants 2025, 14(12), 1461; https://doi.org/10.3390/antiox14121461 (registering DOI)
Submission received: 23 October 2025 / Revised: 2 December 2025 / Accepted: 4 December 2025 / Published: 5 December 2025
(This article belongs to the Special Issue Oxidative Stress in Cardiovascular Diseases)
Versions Notes

Abstract

Doxorubicin (DOX), a clinical broad-spectrum anthracycline chemotherapeutic agent, induces dose-dependent cardiotoxicity that progresses to heart failure (HF), thereby severely limiting its clinical application. Mitochondrial dysfunction and oxidative stress dysregulation are core pathological mechanisms underlying DOX-induced myocardial injury. This study aimed to investigate the protective effect and underlying mechanism of Cistanche deserticola polysaccharides (CDPs) against DOX-induced cardiotoxicity in C57BL/6J mice. Compared with the DOX model group, CDPs significantly increased left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS), and reduced the activities of serum creatine kinase (CK), creatine kinase-MB (CK-MB), and lactate dehydrogenase (LDH). Additionally, CDPs notably decreased the malondialdehyde (MDA) levels in serum and myocardial tissue, while significantly enhancing the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Moreover, CDPs ameliorated mitochondrial swelling and crista fracture, upregulated the expression of mitochondrial respiratory chain complex-related genes, and increased adenosine triphosphate (ATP) production. In conclusion, CDPs alleviate DOX-induced cardiotoxicity and protect cardiac function by inhibiting myocardial oxidative stress and improving mitochondrial function, which provides a potential therapeutic strategy for preventing DOX-related cardiotoxicity.
Keywords: DOX-induced cardiotoxicity; Cistanche deserticola polysaccharides; antioxidant activity; mitochondrial structure; mitochondrial respiration DOX-induced cardiotoxicity; Cistanche deserticola polysaccharides; antioxidant activity; mitochondrial structure; mitochondrial respiration

Share and Cite

MDPI and ACS Style

Qi, J.; Zhang, Y.; Cui, M.; Shi, Y.; Luo, X.; Fan, C.; Wan, S.; An, P.; Luo, Y.; Luo, J. Cistanche deserticola Polysaccharides Protect Against Doxorubicin-Induced Cardiotoxicity via Antioxidant and Mitochondrial Mechanisms. Antioxidants 2025, 14, 1461. https://doi.org/10.3390/antiox14121461

AMA Style

Qi J, Zhang Y, Cui M, Shi Y, Luo X, Fan C, Wan S, An P, Luo Y, Luo J. Cistanche deserticola Polysaccharides Protect Against Doxorubicin-Induced Cardiotoxicity via Antioxidant and Mitochondrial Mechanisms. Antioxidants. 2025; 14(12):1461. https://doi.org/10.3390/antiox14121461

Chicago/Turabian Style

Qi, Jingyi, Yang Zhang, Mingyang Cui, Yufang Shi, Xinyu Luo, Chang Fan, Sitong Wan, Peng An, Yongting Luo, and Junjie Luo. 2025. "Cistanche deserticola Polysaccharides Protect Against Doxorubicin-Induced Cardiotoxicity via Antioxidant and Mitochondrial Mechanisms" Antioxidants 14, no. 12: 1461. https://doi.org/10.3390/antiox14121461

APA Style

Qi, J., Zhang, Y., Cui, M., Shi, Y., Luo, X., Fan, C., Wan, S., An, P., Luo, Y., & Luo, J. (2025). Cistanche deserticola Polysaccharides Protect Against Doxorubicin-Induced Cardiotoxicity via Antioxidant and Mitochondrial Mechanisms. Antioxidants, 14(12), 1461. https://doi.org/10.3390/antiox14121461

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