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

Title
Carbon monoxide releasing molecule-2 protects mice against acute kidney injury through inhibition of ER stress
Authors
Uddin, Md JamalPak, Eun SeonHa, Hunjoo
Ewha Authors
하헌주Md Jamal Uddin
SCOPUS Author ID
하헌주scopus
Issue Date
2018
Journal Title
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
ISSN
1226-4512JCR Link

2093-3827JCR Link
Citation
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY vol. 22, no. 5, pp. 567 - 575
Keywords
Acute kidney injuryCarbon monoxideER stressOxidative stress
Publisher
KOREAN JOURNAL OF PHYSIOLOGY &

PHARMACOLOGY
Indexed
SCIE; SCOPUS; KCI WOS scopus
Document Type
Article
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.
DOI
10.4196/kjpp.2018.22.5.567
Appears in Collections:
약학대학 > 약학과 > Journal papers
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