Literature DB >> 30090438

Salvianolic acid B protects against doxorubicin induced cardiac dysfunction via inhibition of ER stress mediated cardiomyocyte apoptosis.

Rongchang Chen1, Guibo Sun1,2, Longpo Yang3, Jian Wang3, Xiaobo Sun1,2.   

Abstract

Salvia miltiorrhiza Bunge is a well-known medicinal plant in China. Salvianolic acid B (Sal B) is the most abundant bioactive compound extracted from the root of S. miltiorrhiza. The present study investigates the effect of Sal B on cardiac function and cardiomyocyte apoptosis in doxorubicin (DOX)-treated mice. After pretreatment with Sal B (2 mg kg-1 iv) for 7 d, male BALB/c mice were injected with a single dose of DOX (20 mg kg-1 ip). The cardioprotective effect of Sal B was observed on the 7th day after DOX treatment. DOX caused retarded body growth, apoptotic damage, and Bcl-2 expression disturbance. In contrast, Sal B pretreatment (2 mg kg-1 iv before DOX administration) attenuated the DOX induced apoptotic damage in heart tissues. Further study indicated that Sal B protected against DOX induced cardiotoxicity, at least, partially, by inhibiting endoplasmic reticulum stress, and by being involved in the PI3K/Akt pathway. These findings clarified the potential of Sal B as a promising reagent for treating DOX induced cardiotoxicity.

Entities:  

Year:  2016        PMID: 30090438      PMCID: PMC6062089          DOI: 10.1039/c6tx00111d

Source DB:  PubMed          Journal:  Toxicol Res (Camb)        ISSN: 2045-452X            Impact factor:   3.524


  42 in total

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  9 in total

1.  Cardiomyocyte Stim1 Deficiency Exacerbates Doxorubicin Cardiotoxicity by Magnification of Endoplasmic Reticulum Stress.

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Review 3.  The Research Progress of Trastuzumab-Induced Cardiotoxicity in HER-2-Positive Breast Cancer Treatment.

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4.  Effects and Mechanism of Salvianolic Acid B on the Injury of Human Renal Tubular Epithelial Cells Induced by Iopromide.

Authors:  Shu-Jun Dong; Xin-Yue Gao; Ming-Xin Pei; Ting Luo; Dong Fan; Yan-Ling Chen; Jun-Feng Jin; Xiao-Duo Zhao
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5.  Upregulation of serum and glucocorticoid-regulated kinase 1 (SGK1) ameliorates doxorubicin-induced cardiotoxic injury, apoptosis, inflammation and oxidative stress by suppressing glucose regulated protein 78 (GRP78)-mediated endoplasmic reticulum stress.

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6.  Didymin attenuates doxorubicin-induced cardiotoxicity by inhibiting oxidative stress.

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  9 in total

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