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Journal of Chinese Pharmaceutical Sciences ›› 2019, Vol. 28 ›› Issue (1): 10-20.DOI: 10.5246/jcps.2019.01.002

• Original articles • Previous Articles     Next Articles

Proteomic changes in rat kidney injured by adenine and the regulation of anemoside B4

Luling He1,2#, Qin Gong1,2#, Xuan Yu3, Mulan Wang2, Shasha Wong2, Fan Lei3, Hongwei Gao4, Yingying Luo1,2, Yulin Feng1,2, Shilin Yang1,2, Jun Li1,2*, Lijun Du2,3*   

  1. 1. Jiangxi University of Traditional Chinese Medicine, Nanchang 330006, China
    2. State Key Laboratory of Innovative Drugs and Efficient Energy-saving Pharmaceutical Equipment, Nanchang 330006, China
    3. School of Life Sciences, Tsinghua University, Beijing 100084, China
    4. College of Pharmacy, Guangxi University of Chinese Medicine, Nanning 530000, China
  • Received:2018-11-19 Revised:2018-12-19 Online:2019-01-27 Published:2018-12-26
  • Contact: Tel.: +86-18070090101; +86-13810460205, E-mail: 21363492@qq.com; lijundu@mail.tsinghua.edu.cn
  • Supported by:

    National Innovative Drugs 13th Five-Year Major Special Project of China (Grant No. 2018ZX09301030-002).

Abstract:

Adenine is commonly used to establish the animal models for chronic kidney injury and its renal interstitial fibrosis. As an endogenous substance, adenine-induced kidney damage has not yet been fully studied and elucidated, except for inflammatory reaction. Here we analyzed the proteomics of kidney of rats after adenine overloading using LS-MS/MS assay, and observed the role of anemoside B4 (B4). The results showed that adenine could down-regulate 285 proteins and up-regulate 164 proteins in rat kidney tissue compared with the normal group. Down-regulated proteins mainly affected related pathways, such as energy metabolism, while up-regulated proteins affected inflammatory response pathways and metabolic pathways. B4 could significantly reverse the down-regulation of about 40 proteins, which were involved in mitochondria, redox processes, extracellular exosomes, acetylation and other signaling pathways. Simultaneously, B4 could inhibit the up-regulation of five proteins caused by adenine, which were involved in cell cycle, oocyte meiosis, PI3K-Akt and other signaling pathways. Further experimental results of mRNA expression using real-time PCR assay supported the proteomic analysis. Therefore, we proposed that the damage of rat kidney caused by adenine was more complicated, not only with an inflammatory reaction, but also with extensive effects to various metabolic processes in the body. This work provided a valuable clue for comprehensive understanding of adenine-induced renal damage.

Key words: Adenine, Chronic kidney injury, Proteome, Anemoside B4, Rat

CLC Number: 

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