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NMCP-2 polysaccharide purified from Morchella conica effectively prevents doxorubicin-induced cardiotoxicity by decreasing cardiomyocyte apoptosis and myocardial oxidative stress

文献类型： 外文期刊

作者： Xu, Na 1 ; Lu, Yi 2 ; Yao, Xinmiao 1 ; Zhao, Rui 1 ; Li, Zhebin 1 ; Li, Jialei 1 ; Zhang, Yinglei 1 ; Li, Bo 1 ; Zhou, Ye 1 ; S 1 ;

作者机构： 1.Heilongjiang Acad Agr Sci, Inst Food Proc, Harbin 150000, Heilongjiang, Peoples R China

2.Jilin Univ, Coll Vet Med, Inst Zoonosis, Key Lab Zoonosis Res,Minist Educ, Changchun 130062, Peoples R China

关键词： cardiotoxicity; doxorubicin; mitochondrial apoptosis; NMCP-2; oxidative stress

期刊名称：FOOD SCIENCE & NUTRITION （ 2020影响因子：2.863； 五年影响因子：3.141 ）

ISSN： 2048-7177

年卷期： 2021 年 9 卷 11 期

页码：

收录情况： SCI

摘要： Doxorubicin (DOX) is an anthracycline antibiotic used in the clinical treatment of cancer, but its use is limited due to its cardiotoxic effects. Therefore, it is necessary to explore natural compounds that are effective in protecting against the cardiotoxicity caused by DOX. Neutral Morchella conica polysaccharides-2 (NMCP-2) is a natural polysaccharide with antioxidant activity that was isolated and purified from Morchella conica in our laboratory's previous study. This study aimed to investigate the possible protective effect of NMCP-2 on DOX-induced cardiotoxicity and the potential underlying mechanisms. The model of DOX-induced H9C2 cells and the model of DOX-induced mice were used in this study. In in vitro studies of H9C2 myocardial cells, NMCP-2 effectively increased the activity of H9C2 cells, reducing the levels of lactate dehydrogenase (LDH). In the mouse model of DOX-induced chronic cardiotoxicity, NMCP-2 significantly reduced the cardiac index, reduced the release of serum cardiac enzymes, and improved the pathology of murine myocardial tissues, thereby alleviating DOX-induced cardiotoxicity. Further mechanism studies showed that pretreatment with NMCP-2 counteracted the oxidative stress induced by DOX, as indicated by increasing superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) activities, and malondialdehyde (MDA) production decreased. In addition, we observed NMCP-2 inhibited the activation of the mitochondrial apoptosis pathway and regulated the disordered expression of Bcl-2 and Bax in the myocardial tissues of DOX-treated mice. These findings indicated that NMCP-2, a natural bioactive compound, could potentially be used as a food supplement to reduce the cardiotoxicity caused by DOX.

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