ArticleInternational journal of clinical and experimental pathology2015
Correlation between proinflammatory role of a lectin from Typhonium giganteum Engl. and macrophage.
Article in International journal of clinical and experimental pathology, 2015. 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.
- Utilizing ultrasound for the extraction of polysaccharides from the tuber of Typhonium giganteum Engl.: Extraction conditions, structural characterization and bioactivities.Ultrasonics sonochemistry · 2025Article
- Typhonium giganteum Lectin Exerts A Pro-Inflammatory Effect on RAW 264.7 via ROS and The NF-κB Signaling Pathway.Toxins · 2017Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo analyze the correlation between proinflammatory effects of a lectin from Typhonium giganteum Engl. and macrophage.
methodsT. giganteum lectin (TGL) was extracted from the tuber of T. giganteum and purified, and was then identified by using SDS-PAGE gel electrophoresis in combination with mass spectrometry. The morphologic changes of macrophage after being stimulated by TGL were observed with scanning electron microscopy. The influences of such stimulation on neutrophil migration were evaluated by establishing an in vitro macrophage-neutrophil co-culture migration model. By establishing a rat peritoneal macrophage in vitro cultured model, the effects of TGL stimulation on inflammatory factors TNF-α and IL-1β released by macrophage were analyzed. With p65 as the index, the expressions of the NF-κB signaling pathway in the cytoplasm and nucleus were detected before and after TGL stimulation respectively. Furthermore, we also investigated whether the inhibitor for NF-κB signaling pathway BAY11-7082 can block p65 nuclear translocation.
resultsAfter being stimulated by TGL, macrophage had increased volume, number of pseudopodia and gradually cracked cell membrane, accompanied by evidently induced migration of neutrophils due to released inflammatory factors. As the concentration of TGL varied, NF-κB's monomer p65 had different expression levels in the cytoplasm and nucleus, while BAY11-7082 can indeed block the nuclear translocation of p65.
conclusionsTGL-induced inflammation was closely related to macrophage mediation.
Indexed as
Identifiers
26617695PMC4637780W2181877452What OpenQuestion holds
Registered trials
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