ArticlePediatric research2019
Caspase-1 involves in bilirubin-induced injury of cultured rat cortical neurons.
Article in Pediatric research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Integrated analysis of UGT1A1 promoter polymorphism, gene expression, and IL-1β reveals genotype-driven susceptibility in Gilbert syndrome.Molecular biology reports · 2026Article
- Parthenolide ameliorates bilirubin-induced neuronal cell injury by mediating autophagy.Experimental brain research · 2026Article
- Visualization of Unconjugated Bilirubin In Vivo with a Novel Approach Using Chemical Exchange Saturation Transfer Magnetic Resonance Imaging in a Rat Model.ACS chemical neuroscience · 2024Article
- [Role of pyroptosis in bilirubin-induced microglial injury].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBilirubin encephalopathy, the most serious complication of hyperbilirubinemia during the neonatal period, with high mortality and morbidity, often causes irreversible neurological damage. Currently, caspase-1, a member of the cysteinyl aspartate-specific protease caspase family, is regarded as a key mediator of inflammatory processes, attracting widespread attention. The purpose of this study was to investigate whether caspase-1 is involved in bilirubin-induced neuronal injury.
methodsVX-765, a highly potent and selective inhibitor of caspase-1, was used to investigate the effects of unconjugated bilirubin (UCB) on rat cortical neurons, including cell viability, morphological changes in the cell membrane, and nuclear factor-kappa B (NF-κB) activation.
resultsNeurons treated with UCB showed increased caspase-1 activity without the secretion of interleukin (IL)-1β and IL-18, and caspase-1 was significantly inhibited by pretreatment with VX-765. The cell viability of the VX-765-pretreated neurons was improved, and cell membrane rupture was prevented, as detected by lactate dehydrogenase release and ethidium bromide uptake. Moreover, NF-κB activation by UCB exposure, was attenuated by VX-765 pretreatment.
conclusionBilirubin-induced neuronal injury involves the activation of caspase-1 and NF-κB, leading to membrane leakage, independently of IL-1β and IL-18.
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