Creatine phosphate disodium salt protects against Dox-induced cardiotoxicity by increasing calumenin

被引:8
|
作者
Wang, Yu [1 ,4 ]
Sun, Ying [3 ]
Guo, Xin [1 ,4 ]
Fu, Yao [1 ,4 ]
Long, Jie [1 ,4 ]
Wei, Cheng-Xi [1 ,4 ]
Zhao, Ming [1 ,2 ,4 ]
机构
[1] Inner Mongolia Univ Nationalities, 22 Holin He St, Tongliao 028002, Inner Mongolia, Peoples R China
[2] Inner Mongolia Univ Nationalities, Affiliated Hosp, 1472 Holin He St, Tongliao 028002, Inner Mongolia, Peoples R China
[3] Capital Med Univ, Ctr Radiat, Beijing Shijitan Hosp, Beijing, Peoples R China
[4] Inner Mongolia Key Lab Mongolian Med Pharmacol Ca, Tongliao, Inner Mongolia, Peoples R China
基金
中国国家自然科学基金;
关键词
Creatine phosphate disodium salt; Doxorubicin; Endoplasmic reticulum stress; ENDOPLASMIC-RETICULUM STRESS; HEART-FAILURE; APOPTOSIS; CELLS;
D O I
10.1007/s00795-017-0176-5
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Inhibiting endoplasmic reticulum stress (ERS)-induced apoptosis may be a new therapeutic target in cardiovascular diseases. Creatine phosphate disodium salt (CP) has been reported to have cardiovascular protective effect, but its effects on ERS are unknown. The aim of this study was to identify the mechanism by which CP exerts its cardioprotection in doxorubicin (Dox)-induced cardiomyocytes injury. In our study, neonatal rats cardiomyocytes (NRC) was randomly divided into control group, model group, and treatment group. The cell viability and apoptosis were detected. grp78, grp94, and calumenin of the each group were monitored. To investigate the role of calumenin, Dox-induced ERS was compared in control and down-regulated calumenin cardiomyocytes. Our results showed that CP decreased Dox-induced apoptosis and relieved ERS. We found calumenin increased in Dox-induced apoptosis with CP. ERS effector C/EBP homologous protein was down-regulated by CP and it was influenced by calumenin. CP could protect NRC by inhibiting ERS, this mechanisms may be associated with its increasing of calumenin.
引用
收藏
页码:96 / 101
页数:6
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