NLRP3 inflammasome mediates contrast media-induced acute kidney injury by regulating cell apoptosis

Iodinated contrast media serves as a direct causative factor of acute kidney injury (AKI) and is involved in the progression of cellular dysfunction and apoptosis. Emerging evidence indicates that NLRP3 inflammasome triggers inflammation, apoptosis and tissue injury during AKI. Nevertheless, the und...

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Published in:Scientific reports 2016-10, Vol.6 (1), p.34682-34682, Article 34682
Main Authors: Shen, Jianxiao, Wang, Ling, Jiang, Na, Mou, Shan, Zhang, Minfang, Gu, Leyi, Shao, Xinghua, Wang, Qin, Qi, Chaojun, Li, Shu, Wang, Wanpeng, Che, Xiajing, Ni, Zhaohui
Format: Article
Language:English
Subjects:
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Apoptosis
Clonal deletion
Contrast agents
Contrast media
Humanities and Social Sciences
Inflammasomes
Inflammation
Kidneys
multidisciplinary
Nephrectomy
Purchasing groups
Science
Secretion
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Summary:Iodinated contrast media serves as a direct causative factor of acute kidney injury (AKI) and is involved in the progression of cellular dysfunction and apoptosis. Emerging evidence indicates that NLRP3 inflammasome triggers inflammation, apoptosis and tissue injury during AKI. Nevertheless, the underlying renoprotection mechanism of NLRP3 inflammasome against contrast-induced AKI (CI-AKI) was still uncertain. This study investigated the role of NLRP3 inflammasome in CI-AKI both in vitro and in vivo . In HK-2 cells and unilateral nephrectomy model, NLRP3 and NLRP3 inflammasome member ASC were significantly augmented with the treatment of contrast media. Moreover, genetic disruption of NLRP3 notably reversed contrast-induced expression of apoptosis related proteins and secretion of proinflammatory factors, similarly to the effects of ASC deletion. Consistent with above results, absence of NLRP3 in mice undergoing unilateral nephrectomy also protected against contrast media-induced renal cells phenotypic alteration and cell apoptosis via modulating expression level of apoptotic proteins. Collectively, we demonstrated that NLRP3 inflammasome mediated CI-AKI through modulating the apoptotic pathway, which provided a potential therapeutic target for the treatment of contrast media induced acute kidney injury.
ISSN:2045-2322
2045-2322
DOI:10.1038/srep34682