Evidence map›Paper›PMID 27146412›Full record

ArticleDigestive diseases and sciences2016

Resveratrol Protects Oxidative Stress-Induced Intestinal Epithelial Barrier Dysfunction by Upregulating Heme Oxygenase-1 Expression.

Na Wang, Qing Han, Gai Wang, Wei-Ping Ma, Jia Wang, Wen-Xin Wu, Yu Guo, Li Liu, Xiao-Yu Jiang, Xiao-Li Xie and 1 more

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 100 citations in OpenAlex.

  1. Review
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  6. [Research progress on the role of resveratrol in wound healing].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2024
    Review
  7. Article
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  10. Crosstalk between Resveratrol and Gut Barrier: A Review.International journal of molecular sciences · 2022
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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

11 authors at 3 institutions in 2 countries.

Na WangDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Medical University, Hebei Institute of Gastroenterology, No. 215 Heping West Road, Shijiazhuang, 050000, Hebei, China.
Qing HanDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Medical University, Hebei Institute of Gastroenterology, No. 215 Heping West Road, Shijiazhuang, 050000, Hebei, China.
Gai WangDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Medical University, Hebei Institute of Gastroenterology, No. 215 Heping West Road, Shijiazhuang, 050000, Hebei, China.
Wei-Ping MaDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Medical University, Hebei Institute of Gastroenterology, No. 215 Heping West Road, Shijiazhuang, 050000, Hebei, China.
Jia WangDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Medical University, Hebei Institute of Gastroenterology, No. 215 Heping West Road, Shijiazhuang, 050000, Hebei, China.
Wen-Xin WuDepartment of Pathology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
Yu GuoDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Medical University, Hebei Institute of Gastroenterology, No. 215 Heping West Road, Shijiazhuang, 050000, Hebei, China.
Li LiuDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Medical University, Hebei Institute of Gastroenterology, No. 215 Heping West Road, Shijiazhuang, 050000, Hebei, China.
Xiao-Yu JiangDepartment of Anatomy and Cell Biology, Wayne State University School of Medicine, Detroit, MI, USA.
Xiao-Li XieDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Medical University, Hebei Institute of Gastroenterology, No. 215 Heping West Road, Shijiazhuang, 050000, Hebei, China.
Hui-Qing JiangDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Gastroenterology, Hebei Medical University, Hebei Institute of Gastroenterology, No. 215 Heping West Road, Shijiazhuang, 050000, Hebei, China. jianghq@aliyun.com.
Hebei Medical University · CNSecond Hospital of Hebei Medical University · CNWayne State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimObstructive jaundice (OJ) is frequently complicated by infections and has been associated with increased bacterial translocation, intestinal epithelial hyperpermeability, and oxidative stress, but the mechanism remains unclear. The potential effect of resveratrol (Res) on modifying intestinal epithelial dysfunction was evaluated both in vitro and in vivo.

methodsCaco-2 cells (in vitro) and male Wistar rats (n = 60; in vivo) were used to evaluate the role of Res on intestinal epithelial dysfunction. Hydrogen peroxide was used to induce oxidative stress in the Caco-2 cells. In bile duct-ligated group, OJ was successfully established on Day 7 after bile duct ligation, whereas sham-operated and vehicle-treated rats served as controls. Western blot and RT-qPCR were performed to analyze TJ proteins expression in epithelium isolated from rat intestine.

resultsIntestinal hyperpermeability was associated with decreased expression and phosphorylation of occludin and zonula occluden (ZO-1), but increased oxidation in Caco-2 cells and the intestinal epithelium. Res treatment increased the epithelial expression and phosphorylation of occludin and ZO-1 in a concentration-dependent manner. Moreover, Res which protected Caco-2 cells from H2O2-induced oxidative damage clearly reduced malondialdehyde level and intracellular reactive oxygen species accumulation, but increased the expression levels of superoxide dismutase and heme oxygenase-1 (HO-1). Further studies showed that Res also inhibited H2O2-induced protein kinase C activity and p38 phosphorylation. Interestingly, these effects of Res were abolished by the HO-1 inhibitor zinc protoporphyrin or knockdown of HO-1 by siRNA.

conclusionsRes protected gut barrier function possibly by initiating HO-1-dependent signaling which is essential for common expression of key tight junction proteins. It also provides a rationale to develop Res clinical applications of intestinal disorders.

Indexed as

AnimalsAntioxidantsBile DuctsBlotting, WesternCaco-2 CellsHeme Oxygenase-1HumansHydrogen PeroxideIntestinal MucosaIn Vitro TechniquesJaundice, ObstructiveLigationMaleMalondialdehydeOccludinOxidative StressAntioxidantsHeme Oxygenase-1Hydrogen PeroxideMalondialdehydeOccludinProtein Kinase CReactive Oxygen SpeciesResveratrolRNA, MessengerStilbenesZonula Occludens-1 ProteinIntestinal mucosal barrierObstructive jaundiceResveratrolTight junction

Identifiers

PMID27146412
OpenAlexW2345400600

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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.