Evidence map›Paper›PMID 28421347›Full record

ArticleSurgery today2017

TU-100 exerts a protective effect against bacterial translocation by maintaining the tight junction.

Chie Takasu, Wubetu Gizachew Yismaw, Nobuhiro Kurita, Kozo Yoshikawa, Hideya Kashihara, Toru Kono, Mitsuo Shimada

Abstract read
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Article in Surgery today, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Chie TakasuDepartments of Surgery, Institute of Health Biosciences, Tokushima University, Kuramoto 3-18-15, Tokushima, 770-8503, Japan. takasu.chie@tokushima-u.ac.jp.
Wubetu Gizachew YismawDepartments of Surgery, Institute of Health Biosciences, Tokushima University, Kuramoto 3-18-15, Tokushima, 770-8503, Japan.
Nobuhiro KuritaDepartments of Surgery, Institute of Health Biosciences, Tokushima University, Kuramoto 3-18-15, Tokushima, 770-8503, Japan.
Kozo YoshikawaDepartments of Surgery, Institute of Health Biosciences, Tokushima University, Kuramoto 3-18-15, Tokushima, 770-8503, Japan.
Hideya KashiharaDepartments of Surgery, Institute of Health Biosciences, Tokushima University, Kuramoto 3-18-15, Tokushima, 770-8503, Japan.
Toru KonoCenter for Clinical and Biomedical Research, Sapporo Hisgashi Tokushukai Hospital, Hokkaido, Japan.
Mitsuo ShimadaDepartments of Surgery, Institute of Health Biosciences, Tokushima University, Kuramoto 3-18-15, Tokushima, 770-8503, Japan.
Tokushima University · JPSapporo Higashi Tokushukai Hospital · JP

Funding

Japan Society for the Promotion of Science Grant-in-Aid for Scientific Research B: No. 237915Japan Society for the Promotion of Science Grant-in-Aid for Scientific Research C: No. 225914
6 · The paper itself

Abstract

purposeWe previously reported that TU-100 suppresses irinotecan hydrochloride (CPT-11)-induced inflammatory cytokines and apoptosis. However, the mechanism underlying this effect has not been fully elucidated. The aim of this study was to further clarify the mechanism of CPT-11-induced bacterial translocation (BT) and the effect of TU-100 on BT.

methodsCell cytotoxicity was assessed in vitro by a WST-8 assay. For the in vivo experiments, rats were randomly divided into 3 groups: the control group, the CPT-11 group (250 mg/kg i.p. for 2 days), and the CPT-11 and TU-100 co-treated group (1000 mg/kg, p.o. for 5 days). All of the rats were sacrificed on day 6 and their tissues were collected.

resultsCPT-11 and TU-100 co-treatment improved CPT-11 the related cytotoxicity in vitro. All CPT-11-treated rats developed different grades of diarrhea and BT was observed in 80% of the rats. CPT-11 caused a significant increase in the expression of TLR4, IL-6, TNF-α, IL-1β and caspase-3 mRNAs in the large intestine. The expression of tight junction (TJ) marker mRNAs (occludin, claudin-1 and 4, and ZO-1) was significantly decreased in comparison to the control group. TU-100 co-treatment significantly reversed diarrhea, BT, and the expression of TLR2, IL-6, TNF-α, IL-1β and caspase-3, and improved the expression of occludin, claudin-4 and ZO-1.

conclusionsTU-100 can suppress the adverse effects associated with CPT-11 and improve the function of the TJ. It is possible that this occurs through the TLR pathway.

Indexed as

AnimalsAntineoplastic Agents, PhytogenicBacterial TranslocationCamptothecinCells, CulturedClaudin-4CytokinesDiarrheaHumansInflammation MediatorsIrinotecanMaleNaphthoquinonesOccludinPhytotherapyRats, Wistar12,13-dihydro-N-methyl-6,11,13-trioxo-5H-benzo(4,5)cyclohepta(1,2-b)naphthalen-5,12-imineAntineoplastic Agents, PhytogenicCamptothecinClaudin-4CytokinesInflammation MediatorsIrinotecanNaphthoquinonesOccludinToll-Like ReceptorsZonula Occludens-1 ProteinInflammatory cytokineKampoToll-like-receptor

Identifiers

PMID28421347
OpenAlexW2605727985

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.