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Published:
Apr 27, 2022DOI:
10.4314/tjpr.v21i2.6Keywords:
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Main Article Content
Down-regulation of NRIP1 alleviates pyroptosis in human lens epithelial cells exposed to hydrogen peroxide by inhibiting NF-κB activation
Abstract
Purpose: To investigate the role of nuclear receptor-interacting protein 1 (NRIP1) in oxidative stressinduced apoptosis and pyroptosis in cataract disease.
Methods: Human lens epithelial cells (HLE-B3 cells) were exposed to hydrogen peroxide (H2O2). NRIP1 expression in hydrogen peroxide (H2O2)-treated HLE-B3 cells was determined by western blotting and quantitative reverse transcription polymerase chain reaction (qRT-PCR). CCK8 and EdU staining were used to assess cell viability. Flow cytometry and western blotting were used to assess pyroptosis.
Results: NRIP1 was significantly up-regulated in HLE-B3 cells post-H2O2 incubation (p < 0.01). Hydrogen peroxide incubation reduced cell viability and proliferation of HLE-B3 cells, while NRIP1 knockdown enhanced cell viability and proliferation. NRIP1 silencing attenuated the H2O2-induced increase in NLRP3, N-terminal domain of gasdermin D, caspase-1, interleukin (IL)-1β, and IL-18 in HLEB3 cells, but suppressed the pyroptosis of H2O2-treated HLE-B3 cells. Hydrogen peroxide incubation down-regulated protein expression of cytoplasmic NF-κB and up-regulated nuclear NF-κB, while the expression of cytoplasmic NF-κB was increased and nuclear NF-κB was decreased in HLE-B3 cells by HLE-B3 interference.
Conclusion: NRIP1 down-regulation represses apoptosis and pyroptosis of H2O2-treated human lens epithelial cells by inhibiting NF-κB activation, thus, providing a potential strategy to treat cataract disease.
