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

被引:35
作者
Chen, Rongchang [1 ]
Sun, Guibo [1 ,3 ]
Yang, Longpo [2 ]
Wang, Jian [2 ]
Sun, Xiaobo [1 ,3 ]
机构
[1] Chinese Acad Med Sci, Peking Union Med Coll, Inst Med Plant Dev, 151 North Rd Malianwa, Beijing 100094, Peoples R China
[2] Harbin Univ Commerce, Xuehai St, Harbin 150028, Heilongjiang, Peoples R China
[3] Zhongguancun Open Lab Res & Dev Nat Med & Hlth Pr, Beijing, Peoples R China
关键词
ISCHEMIA-REPERFUSION INJURY; OXIDATIVE STRESS; REACTIVE OXYGEN; CELL APOPTOSIS; IN-VITRO; AKT; CARDIOTOXICITY; MILTIORRHIZA; ACTIVATION; SUPPRESSION;
D O I
10.1039/c6tx00111d
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
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.
引用
收藏
页码:1335 / 1345
页数:11
相关论文
共 47 条
[1]   Synergistic interaction between lipid-loading and doxorubicin exposure in Huh7 hepatoma cells results in enhanced cytotoxicity and cellular oxidative stress: implications for acute and chronic care of obese cancer patients [J].
AlGhamdi, S. ;
Leoncikas, V. ;
Plant, K. E. ;
Plant, N. J. .
TOXICOLOGY RESEARCH, 2015, 4 (06) :1479-1487
[2]   Acute doxorubicin cardiotoxicity is successfully treated with the phytochemical oleuropein through suppression of oxidative and nitrosative stress [J].
Andreadou, Ioanna ;
Sigala, Fragiska ;
Iliodromitis, Efstathios K. ;
Papaefthimiou, Maria ;
Sigalas, Constantinos ;
Aligiannis, Nektarios ;
Savvari, Paraskevi ;
Gorgoulis, Vassilis ;
Papalabros, Efstathios ;
Kremastinos, Dimitrios. Th. .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2007, 42 (03) :549-558
[3]   Low-dose chemotherapeutic drugs induce reactive oxygen species and initiate apoptosis-mediated genomic instability [J].
Arun, Renganathan ;
Dhivya, Sridaran ;
Abraham, Suresh K. ;
Premkumar, Kumpati .
TOXICOLOGY RESEARCH, 2016, 5 (02) :547-556
[4]  
Chun-Yan S., 2015, CHIN J NAT MED, V13
[5]   MicroRNA-34c-3p is an early predictive biomarker for doxorubicin-induced glomerular injury progression in male Sprague-Dawley rats [J].
Church, Rachel J. ;
McDuffie, J. Eric ;
Sonee, Manisha ;
Otieno, Monicah ;
Ma, Jing Ying ;
Liu, Xuejun ;
Watkins, Paul B. ;
Harrill, Alison H. .
TOXICOLOGY RESEARCH, 2014, 3 (05) :384-394
[6]   Chronic Akt activation attenuated lipopolysaccharide-induced cardiac dysfunction via Akt/GSK3β-dependent inhibition of apoptosis and ER stress [J].
Dong, Maolong ;
Hu, Nan ;
Hua, Yinan ;
Xu, Xihui ;
Kandadi, Machender R. ;
Guo, Rui ;
Jiang, Shasha ;
Nair, Sreejayan ;
Hu, Dahai ;
Ren, Jun .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 2013, 1832 (06) :848-863
[7]   Inhibition of c-Jun-N-terminal Kinase Increases Cardiac Peroxisome Proliferator-activated Receptor α Expression and Fatty Acid Oxidation and Prevents Lipopolysaccharide-induced Heart Dysfunction [J].
Drosatos, Konstantinos ;
Drosatos-Tampakaki, Zoi ;
Khan, Raffay ;
Homma, Shunichi ;
Schulze, P. Christian ;
Zannis, Vassilis I. ;
Goldberg, Ira J. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2011, 286 (42) :36331-36339
[8]   Heat Shock Protein 20 Interacting With Phosphorylated Akt Reduces Doxorubicin-Triggered Oxidative Stress and Cardiotoxicity [J].
Fan, Guo-Chang ;
Zhou, Xiaoyang ;
Wang, Xiaohong ;
Song, Guojie ;
Qian, Jiang ;
Nicolaou, Persoulla ;
Chen, Guoli ;
Ren, Xiaoping ;
Kranias, Evangelia G. .
CIRCULATION RESEARCH, 2008, 103 (11) :1270-U143
[9]   Protective role of Nd1 in doxorubicin-induced cardiotoxicity [J].
Fujimura, L ;
Matsudo, Y ;
Kang, M ;
Takamori, Y ;
Tokuhisa, T ;
Hatano, M .
CARDIOVASCULAR RESEARCH, 2004, 64 (02) :315-321
[10]   Akt promotes survival of cardiomyocytes in vitro and protects against ischemia-reperfusion injury in mouse heart [J].
Fujio, Y ;
Nguyen, T ;
Wencker, D ;
Kitsis, RN ;
Walsh, K .
CIRCULATION, 2000, 101 (06) :660-667