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Int. J. Mol. Sci. 2015, 16(9), 20595-20608;

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

Department of Emergency Medicine, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou 510120, China
Institute of Cardiopulmonary Cerebral Resuscitation, Sun Yat-sen University, Guangzhou 510120, China
Department of Nephrology, the Fourth Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Academic Editor: Paul Evans
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)
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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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