Evidence map›Paper›PMID 27574508›Full record

ArticleFrontiers in pharmacology2016

Propionate Ameliorates Dextran Sodium Sulfate-Induced Colitis by Improving Intestinal Barrier Function and Reducing Inflammation and Oxidative Stress.

Ling-Chang Tong, Yue Wang, Zhi-Bin Wang, Wei-Ye Liu, Sheng Sun, Ling Li, Ding-Feng Su, Li-Chao Zhang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 2% 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

160 citing papers in PubMed, 2 syntheses or guidelines pooled it, 324 citations in OpenAlex.

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100 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 1 country.

Ling-Chang TongDepartment of Pharmacy, Shanghai Municipal Hospital of Traditional Chinese MedicineShanghai, China; Department of Pharmacology, College of Pharmacy, Second Military Medical UniversityShanghai, China.
Yue WangDepartment of Pharmacy, Shanghai Municipal Hospital of Traditional Chinese MedicineShanghai, China; Department of Pharmacy, Ningxia Medical UniversityYinchuan, China.
Zhi-Bin WangDepartment of Pharmacology, College of Pharmacy, Second Military Medical University Shanghai, China.
Wei-Ye LiuDepartment of Pharmacology, College of Pharmacy, Second Military Medical University Shanghai, China.
Sheng SunDepartment of Pharmacology, College of Pharmacy, Second Military Medical University Shanghai, China.
Ling LiDepartment of Pharmacology, College of Pharmacy, Second Military Medical University Shanghai, China.
Ding-Feng SuDepartment of Pharmacology, College of Pharmacy, Second Military Medical University Shanghai, China.
Li-Chao ZhangDepartment of Pharmacy, Shanghai Municipal Hospital of Traditional Chinese Medicine Shanghai, China.
Second Military Medical University · CNShanghai Traditional Chinese Medicine Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Propionate is a short chain fatty acid that is abundant as butyrate in the gut and blood. However, propionate has not been studied as extensively as butyrate in the treatment of colitis. The present study was to investigate the effects of sodium propionate on intestinal barrier function, inflammation and oxidative stress in dextran sulfate sodium (DSS)-induced colitis mice. Animals in DSS group received drinking water from 1 to 6 days and DSS [3% (w/v) dissolved in double distilled water] instead of drinking water from 7 to 14 days. Animals in DSS+propionate (DSS+Prop) group were given 1% sodium propionate for 14 consecutive days and supplemented with 3% DSS solution on day 7-14. Intestinal barrier function, proinflammatory factors, oxidative stress, and signal transducer and activator of transcription 3 (STAT3) signaling pathway in the colon were determined. It was found that sodium propionate ameliorated body weight loss, colon-length shortening and colonic damage in colitis mice. Sodium propionate significantly inhibited the increase of FITC-dextran in serum and the decrease of zonula occludens-1 (ZO-1), occludin, and E-cadherin expression in the colonic tissue. It also inhibited the expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) mRNA and phosphorylation of STAT3 in colitis mice markedly, reduced the myeloperoxidase (MPO) level, and increased the superoxide dismutase and catalase level in colon and serum compared with DSS group. Sodium propionate inhibited macrophages with CD68 marker infiltration into the colonic mucosa of colitis mice. These results suggest that oral administration of sodium propionate could ameliorate DSS-induced colitis mainly by improving intestinal barrier function and reducing inflammation and oxidative stress via the STAT3 signaling pathway.

Indexed as

dextran sulfate sodiuminflammationintestinal barrier functionpropionateshort-chain fatty acidtight junction proteinulcerative colitis

Identifiers

PMID27574508
PMCPMC4983549
OpenAlexW2513148641

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.