Effect of Secreted Frizzled-Related Protein 5 in Mice with Heart Failure

被引:0
|
作者
Hong, Pan [1 ]
Wang, Lijie [1 ]
Wang, Hongchao [1 ]
Shi, Min [2 ]
Guo, Bingyan [1 ,2 ]
机构
[1] Second Hosp Hebei Med Univ, Dept Cardiol, Shijiazhuang 050017, Peoples R China
[2] Hebei Key Lab Lab Med, Shijiazhuang 050017, Peoples R China
基金
中国国家自然科学基金;
关键词
WNT-INHIBITORS; ROLES; SFRP5; EXPRESSION;
D O I
10.1155/2022/1606212
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
Although some progress has been made in its treatment, heart failure is still one of the most important health problems that endanger public health. This study aims to explore the myocardial protective effect of secreted frizzled-related protein 5 (SFRP5) on mice with heart failure. The mouse model of heart failure was established by using the isoproterenol (ISO) hydrochloride gradient modeling method. The treatment group was injected with 0.02 mg/kg/24 h SFRP5 recombinant protein intraperitoneally 30 minutes after the injection of isoproterenol, and the ISO + phosphate-buffered saline (PBS) group was injected with the same amount of PBS. After intraperitoneal injection of SFRP5 recombinant protein in mice with heart failure, the inflammatory response was reduced, and the left ventricular systolic and diastolic function of heart failure mice and the pathological structure of the myocardial tissue were improved. Compared with the ISO group, the expression level of SFRP5 protein in the ISO + SFRP5 group was increased significantly, the expression levels of Wnt5a and JNK protein were decreased markedly, and the enzyme activities of SOD and GSH-Px in the serum were observably increased, but they were lower than those parameters in the normal group. The SFRP5 recombinant protein has a protective effect on isoproterenol-induced heart failure in mice. The mechanism of action may be related to inhibiting the Wnt5A/JNK signaling pathway and reducing oxidative stress and inflammation. SFRP5 may be one of the therapeutic targets of heart failure.
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页数:8
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