ArticleCurrent neurovascular research2022
Heme Oxygenase-1 may Mediate Early Inflammatory Response of Intracerebral Hemorrhage through Toll-like Receptor 4 Signaling Pathway.
Article in Current neurovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Microglial FoxO3a deficiency ameliorates ferroptosis-induced brain injury of intracerebral haemorrhage via regulating autophagy and heme oxygenase-1.Journal of cellular and molecular medicine · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe aim of this study was to investigate whether heme oxygenase-1 (HO-1) promotes an early neuroinflammatory response after intracerebral hemorrhage (ICH) by regulating the toll-like receptor 4 (TLR4) signaling pathway.
methodsWe used a stereotaxic instrument to induce a mouse model of ICH through collagenase. We divided the participants into a control group, an ICH group, and an ICH and zinc protoporphyrin IX (ZnPP) group. The temporal expression pattern and cell localization of HO-1 and TLR4 after the ICH were detected by immunofluorescence and western blot; after the expression of HO-1 was inhibited, the expression levels of the TLR4 protein, the downstream molecule myeloid differentiation factor 88 (MyD88), the Toll and interleukin-1 receptor (TIR) -domain-containing adapter-inducing interferon-β (TRIF) and the inflammatory factors were measured by western blotting.
resultsImmunofluorescence showed that HO-1 and TLR4 had similar temporal expression patterns and cellular localization after ICH, and we found that inhibiting HO-1 reduces the expression of TLR4 protein pathways, including TLR4, MyD88, TRIF, and related inflammatory factors, by studying the inhibitor ZnPP.
conclusionThese results indicate that HO-1 may promote early neuroinflammation after ICH through the TLR4/MyD88/TRIF signaling pathway.
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