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Open AccessArticle

Exogenous Carbon Monoxide Decreases Sepsis-Induced Acute Kidney Injury and Inhibits NLRP3 Inflammasome Activation in Rats

by 1,2,†, 3,†, 1,2, 1, 1, 1,2 and 1,2,*
1
Department of Emergency Medicine, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou 510120, China
2
Institute of Cardiopulmonary Cerebral Resuscitation, Sun Yat-sen University, Guangzhou 510120, China
3
Department of Nephrology, the Fourth Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: Paul Evans
Int. J. Mol. Sci. 2015, 16(9), 20595-20608; https://doi.org/10.3390/ijms160920595
Received: 12 July 2015 / Revised: 11 August 2015 / Accepted: 19 August 2015 / Published: 31 August 2015
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
Carbon monoxide (CO) has shown various physiological effects including anti-inflammatory activity in several diseases, whereas the therapeutic efficacy of CO on sepsis-induced acute kidney injury (AKI) has not been reported as of yet. The purpose of the present study was to explore the effects of exogenous CO on sepsis-induced AKI and nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome activation in rats. Male rats were subjected to cecal ligation and puncture (CLP) to induce sepsis and AKI. Exogenous CO delivered from CO-releasing molecule 2 (CORM-2) was used intraperitoneally as intervention after CLP surgery. Therapeutic effects of CORM-2 on sepsis-induced AKI were assessed by measuring serum creatinine (Scr) and blood urea nitrogen (BUN), kidney histology scores, apoptotic cell scores, oxidative stress, levels of cytokines TNF-α and IL-1β, and NLRP3 inflammasome expression. CORM-2 treatment protected against the sepsis-induced AKI as evidenced by reducing serum Scr/BUN levels, apoptotic cells scores, increasing survival rates, and decreasing renal histology scores. Furthermore, treatment with CORM-2 significantly reduced TNF-α and IL-1β levels and oxidative stress. Moreover, CORM-2 treatment significantly decreased NLRP3 inflammasome protein expressions. Our study provided evidence that CORM-2 treatment protected against sepsis-induced AKI and inhibited NLRP3 inflammasome activation, and suggested that CORM-2 could be a potential therapeutic candidate for treating sepsis-induced AKI. View Full-Text
Keywords: acute kidney injury; carbon monoxide; NLRP3 inflammasome; sepsis acute kidney injury; carbon monoxide; NLRP3 inflammasome; sepsis
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Wang, P.; Huang, J.; Li, Y.; Chang, R.; Wu, H.; Lin, J.; Huang, Z. Exogenous Carbon Monoxide Decreases Sepsis-Induced Acute Kidney Injury and Inhibits NLRP3 Inflammasome Activation in Rats. Int. J. Mol. Sci. 2015, 16, 20595-20608.

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