Evidence map›Paper›PMID 32617860›Full record

ArticleInflammation2020

Inhibition of C3a/C3aR Axis in Diverse Stages of Ulcerative Colitis Affected the Prognosis of UC by Modulating the Pyroptosis and Expression of Caspase-11.

Xiaohua Zhang, Yong Chen, Shuxia Yu, Bingjie Jin, Wenmin Liu

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In one paragraph

Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  3. The complement system in intestinal inflammation and cancer.The Journal of clinical investigation · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Xiaohua ZhangDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan City, 250021, Shandong Province, China.
Yong ChenDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan City, 250021, Shandong Province, China.
Shuxia YuDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan City, 250021, Shandong Province, China.
Bingjie JinDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan City, 250021, Shandong Province, China.
Wenmin LiuDepartment of Dermatology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan City, 250021, Shandong Province, China. wenminliu12@126.com.ORCID http://orcid.org/0000-0002-6469-1264
Shandong Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ulcerative colitis (UC) is a serious digestive system disease. Furthermore, the activation of C3a/C3aR axis promoted the expression of caspase-11. And higher levels of caspase-11 could induce the pyroptosis and inflammation of cells. However, some studies suggested that caspase-11 could promote and suppress the inflammation during the development of UC. In addition, whether C3a/C3aR axis could affect the development of UC by modulating the expression of caspase-11 is unclear. We established the UC rat model in this study. Next, the C3aR inhibitor was used to treat these rats at diverse stages of UC. Next, the HE staining was performed to detect the intestinal damage. ELISA was performed to reveal the expression of IL-6 and TNF-α in different stages of UC. Western blotting was used to detect the expression of caspase-11 and C3aR in different stages of UC. Stimulation of C3aR inhibitor in early stage of UC promoted the expression of C3aR and caspase-11 in later stage of UC. Treatment of C3aR inhibitor in later stage of UC inhibited the expression of C3aR and caspase-11 in later stage of UC. Furthermore, application of C3aR inhibitor in early stage of UC aggravates the damage of colon tissue and enhanced the secretion of TNF-α and IL-6 in the later stage of UC. Treatment of C3aR inhibitor in later stage of UC relieved the symptoms of UC and suppressed the production of TNF-α and IL-6 in the later stage of UC. Application of C3aR inhibitor in early stage of UC induced the poor prognosis of UC by upregulating the expression of caspase-11. Treatment of C3aR inhibitor in later stage of UC relieved the symptoms of UC and lead to the favorable prognosis of UC by inhibiting the expression of caspase-11.

Indexed as

Gene Expression RegulationPyroptosisAnimalsCaspasesColitis, UlcerativeComplement C3aGasderminsInflammationInterleukin-6IntestinesIntracellular Signaling Peptides and ProteinsPhosphate-Binding ProteinsPrognosisRatsRats, Sprague-DawleyReactive Oxygen Speciesanaphylatoxin receptor C3a, ratCasp4 protein, ratCaspasesComplement C3aGasderminsGsdmd protein, ratIl6 protein, ratInterleukin-6Intracellular Signaling Peptides and ProteinsPhosphate-Binding ProteinsReactive Oxygen SpeciesReceptors, G-Protein-CoupledTumor Necrosis Factor-alphaC3a/C3aR axisC3aR inhibitorcaspase-11inflammationulcerative colitis

Identifiers

PMID32617860
OpenAlexW4211149700

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.