Carbon monoxide releasing molecule-2 protects mice against acute kidney injury through inhibition of ER stress

Md Jamal Uddin, Eun Seon Pak, Hunjoo Ha

Research output: Contribution to journalArticlepeer-review

28 Scopus citations


Acute kidney injury (AKI), which is defined as a rapid decline of renal function, becomes common and recently recognized to be closely intertwined with chronic kidney diseases. Current treatment for AKI is largely supportive, and endoplasmic reticulum (ER) stress has emerged as a novel mediator of AKI. Since carbon monoxide attenuates ER stress, the objective of the present study aimed to determine the protective effect of carbon monoxide releasing molecule-2 (CORM2) on AKI associated with ER stress. Kidney injury was induced after LPS (15 mg/kg) treatment at 12 to 24 h in C57BL/6J mice. Pretreatment of CORM2 (30 mg/kg) effectively prevented LPS-induced oxidative stress and inflammation during AKI in mice. CORM2 treatment also effectively inhibited LPS-induced ER stress in AKI mice. In order to confirm effect of CO on the pathophysiological role of tubular epithelial cells in AKI, we used mProx24 cells. Pretreatment of CORM2 attenuated LPS-induced ER stress, oxidative stress, and inflammation in mProx24 cells. These data suggest that CO therapy may prevent ER stress-mediated AKI.

Original languageEnglish
Pages (from-to)567-575
Number of pages9
JournalKorean Journal of Physiology and Pharmacology
Issue number5
StatePublished - Sep 2018

Bibliographical note

Funding Information:
This work is supported by the grants from National Research Foundation (2017R1D1A1B03028835) and Korean Research Fellowship program (2015H1D3A1062189), Republic of Korea.

Publisher Copyright:
Copyright © Korean J Physiol Pharmacol.


  • Acute kidney injury
  • Carbon monoxide
  • ER stress
  • Oxidative stress


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