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A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
Published on: May 16, 2020
Huaier Polysaccharide Attenuates Doxorubicin-Induced Acute Cardiotoxicity by Regulating Ferroptosis
1College of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Abstract:
We studied the effects of Huaier polysaccharide (HP) in doxorubicin-induced myocardial injury in mice. The content of HP in Trametes robiniophila Murr medicinal fungus determined by the phenol-sulfuric acid method was 85.25%. In the in vitro model, the viability of H9c2 cells was significantly increased after HP treatment compared to the control, while doxorubicin (DOX) decreased this parameter. The inhibitory effect of DOX on cell viability was attenuated after HP treatment. In the in vivo model, the body weight of mice in DOX and DOX+HP groups was significantly decreased compared to the control group. ECG showed significantly elevated ST segment in the DOX group, while in the DOX+HP group, ECG was close to normal. The levels of cardiotoxicity markers cTnI and lactate dehydrogenase in the DOX+HP group were significantly lower than in the DOX group. In the DOX group, the myocardial tissue had obvious structural disorder and interfibrillar vacuoles. In the DOX+HP group, the cardiomyocytes were neatly arranged without interfibrillar vacuoles. The expression of the ferroptosis marker glutathione peroxidase 4 was increased in the DOX+HP group compared to the DOX group. Thus, our study reveals that HP attenuated DOX-induced myocardial injury in mice probably by regulating ferroptosis.
Insights
Huaier polysaccharide (HP) protects against doxorubicin-induced heart damage in mice. HP treatment improved cell viability, normalized ECG, and reduced cardiac damage markers, likely by regulating ferroptosis.
Area of Science:
- Pharmacology
- Cardiology
- Biochemistry
Background:
- Doxorubicin (DOX) is a potent chemotherapy agent with known cardiotoxicity.
- Myocardial injury induced by DOX poses a significant clinical challenge.
- Investigating natural compounds for cardioprotective effects is crucial.
Purpose of the Study:
- To evaluate the protective effects of Huaier polysaccharide (HP) against doxorubicin-induced myocardial injury.
- To elucidate the potential mechanism involving ferroptosis regulation.
Main Methods:
- In vitro: H9c2 cell viability assay with DOX and HP treatment.
- In vivo: Mouse model of DOX-induced cardiotoxicity, assessing body weight, ECG, cardiac biomarkers (cTnI, LDH), and myocardial histology.
- Ferroptosis marker (glutathione peroxidase 4) expression analysis.
Main Results:
- HP significantly increased H9c2 cell viability and attenuated DOX-induced cytotoxicity.
- In vivo, HP treatment normalized ECG, reduced cTnI and LDH levels, and improved myocardial structure compared to DOX-only group.
- HP treatment increased the expression of the ferroptosis marker glutathione peroxidase 4.
Conclusions:
- Huaier polysaccharide (HP) demonstrates significant cardioprotective effects against doxorubicin-induced myocardial injury in mice.
- HP likely exerts its protective effects by modulating ferroptosis pathways.
- HP represents a potential therapeutic agent for mitigating chemotherapy-induced cardiotoxicity.
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