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BMC pharmacology & toxicology
01 10, 2023;24 (1): 1.

Cardioprotective effect of crude polysaccharide fermented by Trametes Sanguinea Lyoyd on doxorubicin-induced myocardial injury mice.

Chenjun Shen, Bo Yang, Lili Huang, Yueru Chen, Huajun Zhao, Zhihui Zhu
Author Information
  1. Chenjun Shen: School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, #548 Binwen Road, Hangzhou, 310053, China.
  2. Bo Yang: School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, #548 Binwen Road, Hangzhou, 310053, China.
  3. Lili Huang: School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, #548 Binwen Road, Hangzhou, 310053, China.
  4. Yueru Chen: School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, #548 Binwen Road, Hangzhou, 310053, China.
  5. Huajun Zhao: School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, #548 Binwen Road, Hangzhou, 310053, China. zhj@zcmu.edu.cn.
  6. Zhihui Zhu: School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, #548 Binwen Road, Hangzhou, 310053, China. zhuzhihui@zcmu.edu.cn.
PMID: 36627724 DOI: 10.1186/s40360-022-00641-y

Abstract

Doxorubicin (DOX) is a broad-spectrum anti-tumor drug, but its clinical application is greatly limited because of the cardiotoxicity. Thus, exploration of effective therapies against DOX-induced cardiotoxicity is necessary. The aim of this study is to investigate the effects and possible mechanisms of Trametes Sanguinea Lyoyd fermented crude polysaccharide (TSLFACP) against DOX-induced cardiotoxicity. We investigated the protective effects of TSLFACP on myocardial injury and its possible mechanisms using two in vitro cells of DOX-treated cardiomyocytes H9C2 and embryonic myocardial cell line CCC-HEH-2 and a in vivo mouse model of DOX-induced myocardial injury. We found that TSLFACP could reverse DOX-induced toxicity in H9C2 and CCC-HEH-2 cells. Similarly, we found that when pretreatment with TSLFACP (200 mg/kg, i.g.) daily for 6 days, DOX-induced myocardial damage was attenuated, including the decrease in serum myocardial injury index, and the amelioration in cardiac histopathological morphology. Additionally, immunohistochemistry and western blotting were used to identify the underlying and possible signal pathways. We found that TSLFACP attenuated the expression of LC3-II, Beclin-1 and PRAP induced by DOX. In conclusion, our results demonstrated that TSLFACP could protect against DOX-induced cardiotoxicity by inhibiting autophagy and apoptosis.

Keywords

Cardioprotective effect Cardiotoxicity Doxorubicin Trametes Sanguinea Lyoyd fermented crude polysaccharide

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Grants

  1. 82104448/National Natural Science Foundation of China

MeSH Term

Doxorubicin
Trametes
Apoptosis
Polyporaceae
Oxidative Stress
Mice
Animals
Myocytes, Cardiac
Cardiotoxicity

Chemicals

Doxorubicin
Journal Article Research Support, Non-U.S. Gov't

Word Cloud

Created with Highcharts 10.0.0DOX-inducedTSLFACPmyocardialcardiotoxicityinjurypossibleTrametesSanguineaLyoydfermentedcrudepolysaccharidefoundDoxorubicinDOXeffectsmechanismscellsH9C2CCC-HEH-2attenuatedCardioprotectiveeffectbroad-spectrumanti-tumordrugclinicalapplicationgreatlylimitedThusexplorationeffectivetherapiesnecessaryaimstudyinvestigateinvestigatedprotectiveusingtwovitroDOX-treatedcardiomyocytesembryoniccelllinevivomousemodelreversetoxicitySimilarlypretreatment200 mg/kgigdaily6 daysdamageincludingdecreaseserumindexameliorationcardiachistopathologicalmorphologyAdditionallyimmunohistochemistrywesternblottingusedidentifyunderlyingsignalpathwaysexpressionLC3-IIBeclin-1PRAPinducedconclusionresultsdemonstratedprotectinhibitingautophagyapoptosisdoxorubicin-inducedmiceCardiotoxicity

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