Evidence map›Paper›PMID 29891453›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2018

[Role of caspase-1 activation in bilirubin-induced injury in cultured primary rat hippocampal neurons].

Qian Wei, Jie Feng, Chun-Mei He, Zi-Yu Hua

Abstract read
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 93% of its field
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Qian WeiDepartment of Neonatology, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Chongqing 400014, China.E-mail: 1476595281@qq.com.
Jie Feng
Chun-Mei He
Zi-Yu Hua
China International Science and Technology Cooperation · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the role of caspase-1 activation in bilirubin-induced neuronal injury and the protective effect of VX-765 against bilirubin-induced neurotoxicity in cultured primary rat hippocampal neurons.

methodsCultured primary rat hippocampal neurons were exposed to DMSO (control group), 50 µmol/L bilirubin, or 50 µmol/L bilirubin 1 h after 50 µmol/L VX-765 treatment. The expressions of NLRP3 and caspase-1 in the neurons were detected by Western blotting, and the relative cell survival and death rates were assessed with a modified MTT assay, lactate dehydrogenase assay and Typan blue staining. Interleukin-18 (IL-18) concentration in the culture supernatant was measured using enzyme-linked immunosorbent assay (ELISA).

resultsIn cultured primary rat hippocampal neurons, bilirubin exposure for 3 and 6 h caused significant increases in the expressions of NLRP3 and activated caspase-1 compared with those in the control group (P<0.05). Pretreatment of the cells with VX-765 obviously suppressed bilirubin-induced activation of caspase-1 (P<0.05). The relative survival rate of the neurons was (84.02∓2.31)% in VX-765 intervention group, significantly higher than that in bilirubin group (P<0.05) but lower than that in the control group (P<0.05); LDH release rate in VX-765 intervention group was (10.78∓1.58)%, significantly lower than that in bilirubin group (P<0.05) but higher than that in the control group (P<0.05). The cell death rate in VX-765 intervention group was (5.58∓1.23)%, significantly lower than that in bilirubin group (P<0.05) but higher than that in the control group (P<0.05).

conclusionIn cultured primary rat hippocampal neurons, caspase-1 activation plays a role in bilirubin-induced neurotoxicity, and VX-765 treatment provides protection against bilirubin-induced neuronal injury by inhibiting caspase-1 activation.

Indexed as

HippocampusAnimalsApoptosisBilirubinCaspase 1Caspase 3CaspasesCell DeathCells, CulturedCell SurvivalDimethyl SulfoxideDipeptidesEnzyme ActivationNeuronsNLR Family, Pyrin Domain-Containing 3 Proteinpara-AminobenzoatesbelnacasanBilirubinCaspase 1Caspase 3CaspasesDimethyl SulfoxideDipeptidesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratpara-Aminobenzoates

Identifiers

PMID29891453
PMCPMC6743908
OpenAlexW2811374242

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.