Protective effects of cyclic helix B peptide on aristolochic acid induced acute kidney injury

被引:14
作者
Zeng, Yigang [1 ,2 ]
Zheng, Long [1 ,2 ]
Yang, Zhangru [1 ,2 ]
Yang, Cheng [1 ,2 ]
Zhang, Yi [1 ,2 ]
Li, Jiawei [1 ,2 ]
Zhang, Weitao [1 ,2 ]
Zhang, Mingnan [1 ,2 ]
Hu, Mushuang [1 ,2 ]
Wang, Shuo [1 ,2 ]
Niyazi, Sidikejiang [1 ,2 ]
Xu, Ming [1 ,2 ]
Rong, Ruiming [1 ,2 ]
Zhu, Tongyu [1 ,2 ,3 ]
机构
[1] Fudan Univ, Zhongshan Hosp, Dept Urol, 180 Fenglin Rd, Shanghai 200032, Peoples R China
[2] Shanghai Key Lab Organ Transplantat, Shanghai, Peoples R China
[3] Fudan Univ, Shanghai Publ Hlth Clin Ctr, Shanghai, Peoples R China
基金
中国国家自然科学基金;
关键词
Cyclic Helix B peptide; Aristolochic acid; Acute kidney injury; MITOCHONDRIAL;
D O I
10.1016/j.biopha.2017.07.131
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background: Aristolochic acid (AA) injuries remain a serious condition associated with acute renal dysfunction. Herein, the effect and mechanism of a novel tissue protective peptide, cyclic helical B-peptide (CHBP) derived from erythropoietin, were investigated in a mice model. Methods: Mice were randomly divided into four groups, receiving the following treatments (1: saline; 2: AA 10 mg/kg; 3: AA 10 mg/kg + CHBP 4nmol/kg; 4: AA 10 mg/kg + CHBP 8nmol/kg). Results: Blood urea nitrogen and serum creatinine was increased by AA but decreased by CHBP in a dose-dependent fashion. CHBP also significantly improved renal tubular injury and inflammatory infiltration, which was gradually increased by AA. Apoptotic cells, infiltrating inflammatory cells, and active caspase-3+ cells were greatly reduced by CHBP. In addition, CHBP inhibited caspase-3, 9 and improved bcl-2, bcl-xl protein expression in vivo. Conclusion: Taken together, we demonstrated, for the first time, that CHBP effectively improved renal function and tissue damage caused by AA, which maybe through reducing caspase-3 activation, apoptosis, and inflammation. (C) 2017 Published by Elsevier Masson SAS.
引用
收藏
页码:1167 / 1175
页数:9
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