Carbon monoxide releasing molecule-2 protects mice against acute kidney injury through inhibition of ER stress.
10.4196/kjpp.2018.22.5.567
- Author:
Md Jamal UDDIN
1
;
Eun Seon PAK
;
Hunjoo HA
Author Information
1. Graduate School of Pharmaceutical Sciences, College of Pharmacy, Ewha Womans University, Seoul 03760, Korea. hha@ewha.ac.kr
- Publication Type:Original Article
- Keywords:
Acute kidney injury;
Carbon monoxide;
ER stress;
Oxidative stress
- MeSH:
Acute Kidney Injury*;
Animals;
Carbon Monoxide*;
Carbon*;
Endoplasmic Reticulum;
Epithelial Cells;
Inflammation;
Kidney;
Mice*;
Oxidative Stress;
Renal Insufficiency, Chronic
- From:The Korean Journal of Physiology and Pharmacology
2018;22(5):567-575
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
