Evidence map›Paper›PMID 38916850›Full record

ArticlePharmacological reports : PR2024

A derivative of 3-(1,3-diarylallylidene)oxindoles inhibits dextran sulfate sodium-induced colitis in mice.

Young-Jin Jeong, Hae-Ri Lee, Sun-Ae Park, Joong-Woon Lee, Lee Kyung Kim, Hee Jung Kim, Jae Hong Seo, Tae-Hwe Heo

Abstract read
In one paragraph

Article in Pharmacological reports : PR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

8 authors.

Young-Jin JeongLaboratory of Pharmacoimmunology, Integrated Research Institute of Pharmaceutical Sciences, BK21 FOUR Team for Advanced Program for SmartPharma Leaders, College of Pharmacy, The Catholic University of Korea, NP512, Hall of Cardinal Jin-Suk Cheong, 43 Jibong-Ro, Bucheon-Si, Gyeonggi‑do, 14662, Republic of Korea.
Hae-Ri LeeLaboratory of Pharmacoimmunology, Integrated Research Institute of Pharmaceutical Sciences, BK21 FOUR Team for Advanced Program for SmartPharma Leaders, College of Pharmacy, The Catholic University of Korea, NP512, Hall of Cardinal Jin-Suk Cheong, 43 Jibong-Ro, Bucheon-Si, Gyeonggi‑do, 14662, Republic of Korea.
Sun-Ae ParkLaboratory of Pharmacoimmunology, Integrated Research Institute of Pharmaceutical Sciences, BK21 FOUR Team for Advanced Program for SmartPharma Leaders, College of Pharmacy, The Catholic University of Korea, NP512, Hall of Cardinal Jin-Suk Cheong, 43 Jibong-Ro, Bucheon-Si, Gyeonggi‑do, 14662, Republic of Korea.
Joong-Woon LeeLaboratory of Pharmacoimmunology, Integrated Research Institute of Pharmaceutical Sciences, BK21 FOUR Team for Advanced Program for SmartPharma Leaders, College of Pharmacy, The Catholic University of Korea, NP512, Hall of Cardinal Jin-Suk Cheong, 43 Jibong-Ro, Bucheon-Si, Gyeonggi‑do, 14662, Republic of Korea.
Lee Kyung KimLaboratory of Pharmacoimmunology, Integrated Research Institute of Pharmaceutical Sciences, BK21 FOUR Team for Advanced Program for SmartPharma Leaders, College of Pharmacy, The Catholic University of Korea, NP512, Hall of Cardinal Jin-Suk Cheong, 43 Jibong-Ro, Bucheon-Si, Gyeonggi‑do, 14662, Republic of Korea.
Hee Jung KimLaboratory of Pharmacoimmunology, Integrated Research Institute of Pharmaceutical Sciences, BK21 FOUR Team for Advanced Program for SmartPharma Leaders, College of Pharmacy, The Catholic University of Korea, NP512, Hall of Cardinal Jin-Suk Cheong, 43 Jibong-Ro, Bucheon-Si, Gyeonggi‑do, 14662, Republic of Korea.
Jae Hong SeoLaboratory of Pharmaceutical Manufacturing Chemistry, Integrated Research Institute of Pharmaceutical Sciences, College of Pharmacy, The Catholic University of Korea, 43 Jibong-Ro, Bucheon‑si, Gyeonggi‑do, 14662, Republic of Korea.
Tae-Hwe HeoLaboratory of Pharmacoimmunology, Integrated Research Institute of Pharmaceutical Sciences, BK21 FOUR Team for Advanced Program for SmartPharma Leaders, College of Pharmacy, The Catholic University of Korea, NP512, Hall of Cardinal Jin-Suk Cheong, 43 Jibong-Ro, Bucheon-Si, Gyeonggi‑do, 14662, Republic of Korea. thhur92@catholic.ac.kr.ORCID http://orcid.org/0009-0002-8054-4448

Funding

Basic Science Research Program through the National Research Foundation of Korea 2018R1A6A1A03025108Basic Science Research Program through the National Research Foundation of Korea 2021R1A2C2009782Basic Science Research Program through the National Research Foundation of Korea 2022R1A2C2009911
6 · The paper itself

Abstract

backgroundIA-0130 is a derivative of 3-(1,3-diarylallylidene)oxindoles, which is a selective estrogen receptor modulator (SERM). A previous study demonstrated that SERM exhibits anti-inflammatory effects on colitis by promoting the anti-inflammatory phenotype of monocytes in murine colitis. However, the therapeutic effects of oxindole on colitis remain unknown. Therefore, we evaluated the efficacy of IA-0130 on dextran sulfate sodium (DSS)-induced mouse colitis.

methodsThe DSS-induced colitis mouse model was established by administration of 2.5% DSS for 5 days. Mice were orally administered with IA-0130 (0.01 mg/kg or 0.1 mg/kg) or cyclosporin A (CsA; 30 mg/kg). Body weight, disease activity index score and colon length of mice were calculated and histological features of mouse colonic tissues were analyzed using hematoxylin and eosin staining. The expression of inflammatory cytokines and tight junction (TJ) proteins were analyzed using quantitative real-time PCR and enzyme-linked immunosorbent assay. The expression of interleukin-6 (IL-6) signaling molecules in colonic tissues were investigated using Western blotting and immunohistochemistry (IHC).

resultsIA-0130 (0.1 mg/kg) and CsA (30 mg/kg) prevented colitis symptom, including weight loss, bleeding, colon shortening, and expression of pro-inflammatory cytokines in colon tissues. IA-0130 treatment regulated the mouse intestinal barrier permeability and inhibited abnormal TJ protein expression. IA-0130 down-regulated IL-6 expression and prevented the phosphorylation of signaling molecules in colonic tissues.

conclusionsThis study demonstrated that IA-0130 suppressed colitis progression by inhibiting the gp130 signaling pathway and expression of pro-inflammatory cytokines, and maintaining TJ integrity.

Indexed as

ColitisDextran SulfateOxindolesAnimalsAnti-Inflammatory AgentsColonCytokinesDisease Models, AnimalIndolesInterleukin-6MaleMiceSignal TransductionAnti-Inflammatory AgentsCytokinesDextran SulfateIndolesInterleukin-6OxindolesColitisgp130Intestinal barrierOxindoleSTATTight junction

Identifiers

PMID38916850
PMCPMC11294400

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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.