Knockdown of NLRC5 attenuates renal I/R injury in vitro through the activation of PI3K/Akt signaling pathway.
Biomed Pharmacother
; 103: 222-227, 2018 Jul.
Article
em En
| MEDLINE
| ID: mdl-29655162
ABSTRACT
NLRC5, as the largest member of nucleotide-binding domain and leucine-rich repeat (NLR) family, was involved in various physiological processes, such as inflammation, fibrosis, innate immunity and diabetic nephropathy. However, the role of NLRC5 in acute kidney injury remains unclear. The aim of this study was to investigate the role of NLRC5 in human renal proximal tubular epithelial cells (HK-2) exposed to hypoxia/reoxygenation (H/R). Our results demonstrated that the expression of NLRC5 was significantly up-regulated in HK-2 cells exposed to H/R. Knockdown of NLRC5 significantly improved the viability of HK-2 cells exposed to H/R. In addition, knockdown of NLRC5 efficiently inhibited H/R-induced oxidative stress and apoptosis in HK-2 cells. Mechanistically, knockdown of NLRC5 markedly enhanced the activation of PIK3/Akt signaling pathway in H/R-stimulated HK-2 cells. In summary, our findings indicate that knockdown of NLRC5 attenuates renal I/R injury in vitro through the activation of PI3K/Akt signaling pathway.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Traumatismo por Reperfusão
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Transdução de Sinais
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Fosfatidilinositol 3-Quinases
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Peptídeos e Proteínas de Sinalização Intracelular
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Proteínas Proto-Oncogênicas c-akt
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Técnicas de Silenciamento de Genes
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Rim
Limite:
Humans
Idioma:
En
Revista:
Biomed Pharmacother
Ano de publicação:
2018
Tipo de documento:
Article
País de afiliação:
China