Evidence map›Paper›PMID 27307705›Full record

ArticleDrug design, development and therapy2016

Sulfasalazine inhibits inflammation and fibrogenesis in pancreas via NF-κB signaling pathway in rats with oxidative stress-induced pancreatic injury.

Ya-Ru Wang, Fei-Long Tian, Ming-Xian Yan, Jin-Hua Fan, Li-Yun Wang, Rong-Guang Kuang, Yan-Qing Li

RetractedErratum issuedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Drug design, development and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Drugs and Targets in Fibrosis.Frontiers in pharmacology · 2017
    Review
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Ya-Ru WangDepartment of Gastroenterology, Shandong Qianfoshan Hospital, Shandong University, Ji'nan, Shandong Province, People's Republic of China.
Fei-Long TianShandong University School of Medicine, Qilu Hospital, Shandong University, Ji'nan, Shandong Province, People's Republic of China.
Ming-Xian YanDepartment of Gastroenterology, Shandong Qianfoshan Hospital, Shandong University, Ji'nan, Shandong Province, People's Republic of China.
Jin-Hua FanDepartment of Gastroenterology, Shandong Qianfoshan Hospital, Shandong University, Ji'nan, Shandong Province, People's Republic of China.
Li-Yun WangDepartment of Gastroenterology, Shandong Qianfoshan Hospital, Shandong University, Ji'nan, Shandong Province, People's Republic of China.
Rong-Guang KuangDepartment of Gastroenterology, Shandong Qianfoshan Hospital, Shandong University, Ji'nan, Shandong Province, People's Republic of China.
Yan-Qing LiDepartment of Gastroenterology, Qilu Hospital, Shandong University, Ji'nan, Shandong Province, People's Republic of China.
Shandong Provincial QianFoShan Hospital · CNUniversity Gastroenterology · USQilu Hospital of Shandong University · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPathogenesis and effective therapeutics of chronic pancreatic inflammation and fibrosis remain uncertain. PURPOSE: To investigate the effects of sulfasalazine (SF) on pancreatic inflammation and fibrogenesis.

methodsChronic pancreatic injury in rats was induced by diethyldithiocarbamate (DDC) and interfered by SF through intraperitoneal injection. The rats were divided into five groups: group N, normal control group, rats were treated with dilated water only; group DS1, rats received SF (10 mg/kg) 2 hours before DDC treatment; group DS2, rats were treated with DDC and then SF (100 mg/kg, twice a week); group DS3, rats were treated with DDC, then SF (100 mg/kg, thrice a week); and group DDC, rats were treated with DDC only. Pancreatic inflammation and fibrosis were determined by hematoxylin and eosin staining and Sirius red staining. The genes and proteins related to NF-κB pathway and fibrogenesis including NF-κB/p65, TNF-α, ICAM-1, α-SMA, and Con 1 were detected by immunohistochemical staining, reverse transcription polymerase chain reaction, and Western blotting.

resultsRats in the DDC and DS1 groups showed the highest histological scores after DDC treatment, but the scores of DS2 and DS3 groups decreased significantly when compared with the DDC group. Sirius red staining showed collagen formation clearly in DDC and DS1 rats rather than in DS2 and DS3 rats. NF-κB/p65, ICAM-1, and α-SMA were strongly expressed in DDC and DS1 rats, while DS2 and DS3 rats showed mild to moderate expression by immunohistochemistry. Reverse transcription polymerase chain reaction showed increased levels of NF-κB/p65, ICAM-1, TNF-α, α-SMA, and Con 1 mRNA in DDC and DS1 rats in comparison to normal controls. The mRNA levels of these molecules in DS2 and DS3 rats were significantly lower than those in DS1 and DDC rats. Western blotting demonstrated that the NF-κB/p65, ICAM-1, and α-SMA expressions in pancreatic tissues of the rats of the DDC group were more clear than those of the normal control, DS2, and DS3 rats.

conclusionSF inhibits pancreatic inflammation and fibrogenesis via NF-κB signaling pathway.

Indexed as

Oxidative StressAnimalsFibrosisInflammationInjections, IntraperitonealNF-kappa BPancreasRatsRats, WistarSignal TransductionSulfasalazineNF-kappa BSulfasalazinefibrogenesisinflammationNF-κBpancreatic injurysulfasalazine

Identifiers

PMID27307705
PMCPMC4887069
OpenAlexW2398665448

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.