Evidence map›Paper›PMID 35001346›Full record

ArticleJournal of physiology and biochemistry2022

Procyanidin A1 alleviates DSS-induced ulcerative colitis via regulating AMPK/mTOR/p70S6K-mediated autophagy.

Haihua Zhang, Wuying Lang, Xin Liu, Jiangsong Bai, Qinghui Jia, Qiumei Shi

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of physiology and biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed.

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  17. [Sanguinarine alleviates ulcerative colitis in mice by regulating the Nrf2/NF-κB pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
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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

6 authors.

Haihua Zhang *Hebei Key Laboratory of Specialty Animal Germplasm Resources Exploration and Innovation (Under Planning), Hebei Normal University of Science and Technology, Qinhuangdao, Hebei, 066004, People's Republic of China.
Wuying Lang *College of Biology Pharmacy and Food Engineering, Shangluo University, Shangluo, Shaanxi, 726000, People's Republic of China.
Xin LiuHebei Key Laboratory of Specialty Animal Germplasm Resources Exploration and Innovation (Under Planning), Hebei Normal University of Science and Technology, Qinhuangdao, Hebei, 066004, People's Republic of China.
Jiangsong BaiTechnological Innovation Center for Fur Animal Breeding of Hebei Province, Shijiazhuang, Hebei, 050000, People's Republic of China.
Qinghui JiaHebei Key Laboratory of Preventive Veterinary Medicine, Hebei Normal University of Science and Technology, Qinhuangdao, Hebei, 066004, People's Republic of China.
Qiumei ShiHebei Key Laboratory of Preventive Veterinary Medicine, Hebei Normal University of Science and Technology, Qinhuangdao, Hebei, 066004, People's Republic of China. shiqiumei163@163.com.ORCID http://orcid.org/0000-0002-4882-6309

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ulcerative colitis (UC) is a recurrent chronic inflammatory disease. The symptom of UC is mainly diarrhea including bloody stools. Increasing evidence has suggested that procyanidin A1 (PCA1) exerts an anti-inflammatory effect in several diseases. However, the role of PCA1 in UC is still a mystery. In our study, we explored the effect of PCA1 in dextran sulfate sodium (DSS)-induced UC mice and lipopolysaccharide (LPS)-stimulated HT-29 and IEC-6 cells. Then, cell proliferation, apoptosis, the production of proinflammatory cytokines, and autophagy-related markers were determined. Furthermore, the AMPK/mTOR/p70S6K signaling pathway was assayed by Western blot assay. In in vivo study, we found that PCA1 administration alleviated DSS-induced UC, as evidenced by reducing weight loss, clinical scores, colon weight/length ratio, histological damage, proinflammatory cytokines, and apoptosis. Moreover, we showed that the expression of Beclin-1 and LC3II/I ratio was increased, whereas the level of p62 was decreased after PCA1 treatment in vivo. Meanwhile, the reduced AMP/ATP ratio, enhanced expression of p-AMPK, and decreased p-p70S6K and p-mTOR levels indicate the activation of AMPK/mTOR/p70S6K signaling pathway. In in vitro study, PCA1 promoted cell proliferation and inhibited cell apoptosis in LPS-stimulated HT-29 and IEC-6 cells. Pro-inflammatory cytokines and autophagy-related factors exhibited the same trend as in in vivo results. Mechanically, PCA1 activated the AMPK/mTOR/p70S6K signaling pathway. The treatment with an AMPK inhibitor compound C significantly reversed the anti-inflammatory effect of PCA1 in LPS-stimulated cells. Taken together, these data indicated that PCA1 alleviated UC through induction of AMPK/mTOR/p70S6K-mediated autophagy.

Indexed as

Colitis, UlcerativeRibosomal Protein S6 Kinases, 70-kDaAMP-Activated Protein KinasesAnimalsAutophagyCatechinDextran SulfateMiceProanthocyanidinsTOR Serine-Threonine KinasesAMP-Activated Protein KinasesCatechinDextran SulfateProanthocyanidinsprocyanidin A1Ribosomal Protein S6 Kinases, 70-kDaTOR Serine-Threonine KinasesAutophagyInflammatory bowel disease (IBD)Procyanidin A1 (PCA1)Ulcerative colitis (UC)

Identifiers

PMID35001346

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.