Carbon monoxide releasing molecule-2 protects mice against acute kidney injury through inhibition of ER stress
- 주제(키워드) Acute kidney injury , Carbon monoxide , ER stress , Oxidative stress
- 주제(기타) Pharmacology & Pharmacy; Physiology
- 설명문(일반) [Uddin, Md Jamal; Pak, Eun Seon; Ha, Hunjoo] Ewha Womans Univ, Coll Pharm, Grad Sch Pharmaceut Sci, Seoul 03760, South Korea
- 등재 SCIE, SCOPUS, KCI등재
- 발행기관 KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
- 발행년도 2018
- URI http://www.dcollection.net/handler/ewha/000000156059
- 본문언어 영어
- Published As http://dx.doi.org/10.4196/kjpp.2018.22.5.567
- 저작권 이화여자대학교 논문은 저작권에 의해 보호받습니다.
초록/요약
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.
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