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Abstract
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.
Highlights
Figure 1. si-NLRP3 or si-ASC effect on omnipaque-induced cell apoptosis in HK-2 cells. (a) Quantitative RT-PCR of NLRP3 and ASC
We proposed to investigate the effect of NLRP3 inflammasome activation on CI-Acute kidney injury (AKI) pathogenesis and the underlying mechanism through evaluating proximal renal tubular epithelial cell apoptosis in vitro and in vivo
To evaluate the role of NLRP3 and ASC in contrast-induced AKI (CI-AKI), we first determined whether the levels of NLRP3 and ASC mRNA were influenced by contrast media in HK-2 cell
Summary
Figure 1. si-NLRP3 or si-ASC effect on omnipaque-induced cell apoptosis in HK-2 cells. (a) Quantitative RT-PCR of NLRP3 and ASC. Si-NLRP3 or si-ASC effect on omnipaque-induced cell apoptosis in HK-2 cells. (a) Quantitative RT-PCR of NLRP3 and ASC. HK-2 cells were treated with 20 mg/ml mannitol (Manni.), 250 mgI/ml visipaque (Visip.), and 20 mgI/ml omnipaque (Omnip.) respectively for 72 h. (d) Quantification of cell apoptosis by flow cytometry. HK-2 cells transfected with si-NC or si-NLRP3 or si-ASC were treated with mannitol (Manni., 20 mg/ml), omnipaque (Omnip., 20–40 mgI/ml). Si-ASC and si-NLRP3 dramatically attenuated omnipaque-induced cell apoptosis. We proposed to investigate the effect of NLRP3 inflammasome activation on CI-AKI pathogenesis and the underlying mechanism through evaluating proximal renal tubular epithelial cell apoptosis in vitro and in vivo
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