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International Urology and Nephrology

, Volume 52, Issue 1, pp 187–196 | Cite as

Myricitrin protects against cisplatin-induced kidney injury by eliminating excessive reactive oxygen species

  • Ruiqian Li
  • Libing Hu
  • Chen Hu
  • Qiling Wang
  • Yonghong Lei
  • Bin ZhaoEmail author
Nephrology - Original Paper
  • 36 Downloads

Abstract

Background

Cisplatin could result in a wide range of kidney injuries. During the pathogenetic process, the excessive generation of reactive oxygen species (ROS) induced by cisplatin has been regarded as the initial and critical role, by which DNA damage and cell death could subsequently come up. Therefore the elimination of ROS has long been considered as effective mean to prevent cisplatin-induced kidney injury. Myricitrin is a newfound natural polyphenol hydroxy flavonoid glycoside compound, whose forceful anti-oxidative properties had been confirmed. Thus, we aim to investigate if myricitrin could protect against cisplatin-induced kidney injury.

Methods

A cisplatin-induced kidney injury model was established in mice by intraperitoneal injection of cisplatin. The protective effect of myricitrin on kidney injury was evaluated by serum BUN and Cre level. The Kidney pathology was observed with H&E and TUNEL staining. Then cell viability and apoptosis rate were measured using MMT assay and flow cytometry to assess if myricitrin could protect KH-2 cells against cisplatin-induced injury. The intracellular ROS was detected by ROS fluorogenic probe and quantitatively analyzed by flow cytometry. Finally, the expression of Bcl-2 and Bax was investigated by western blotting to indicate the influence in apoptosis pathway.

Results

Myricitrin could significantly remit kidney injury induced by cisplatin and inhibit apoptosis of KH-2 cells. In mechanism, myricitrin could eliminate ROS and subsequently block activation of apoptosis pathway.

Conclusion

Myricitrin protects against cisplatin-induced kidney injury by eliminating excessive ROS.

Keywords

Cisplatin-induced kidney injury Myricitrin Reactive oxygen species Apoptosis Apoptosis pathway 

Notes

Author contributions

The author contributions were as follows: BZ designed the study; RL drafted the manuscript; The experiments were finished by RL, LH,CH,QW; the data analysis and interpretation involved QW and YL. All authors read and approved the final manuscript.

Compliance with ethical standards

Ethics approval and consent to participate

All animal experiments conformed to the National Institute of Health Guide for the Care and Use of Laboratory Animals’ (NIH Publication No. 85-23, National Academy Press, Washington, DC, revised 1996), with the approval of the Laboratory Animal Center of Kunming Medical University. The approval ID for this study was 20181092.

Conflict of interest

The authors declare that they have no competing interests.

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Copyright information

© Springer Nature B.V. 2019

Authors and Affiliations

  • Ruiqian Li
    • 1
  • Libing Hu
    • 1
  • Chen Hu
    • 1
  • Qiling Wang
    • 1
  • Yonghong Lei
    • 1
  • Bin Zhao
    • 1
    Email author
  1. 1.Department of UrologyThe Third Affiliated Hospital of Kunming Medical UniversityKunmingChina

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