Evidence map›Paper›PMID 36401777›Full record

ArticleArchives of pharmacal research2022

6'-Sialylactose abolished lipopolysaccharide-induced inflammation and hyper-permeability in endothelial cells.

Dung Van Nguyen, Thuy Le Lam Nguyen, Yujin Jin, Lila Kim, Chang-Seon Myung, Kyung-Sun Heo

Abstract read
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In one paragraph

Article in Archives of pharmacal research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Protective effect of 6'-Sialyllactose on LPS-induced macrophage inflammationThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
    Article
  7. Review
  8. Article
  9. Article
  10. Experimental model and novel therapeutic targets for non-alcoholic fatty liver disease development.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023
    Review
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 at 1 institution in 1 country.

Dung Van NguyenCollege of Pharmacy and Institute of Drug Research and Development, Chungnam National University, Daejeon, 34134, South Korea.
Thuy Le Lam NguyenCollege of Pharmacy and Institute of Drug Research and Development, Chungnam National University, Daejeon, 34134, South Korea.
Yujin JinCollege of Pharmacy and Institute of Drug Research and Development, Chungnam National University, Daejeon, 34134, South Korea.
Lila KimGeneChem Inc. A-201, 187 Techno 2-ro, Daejeon, 34025, South Korea.
Chang-Seon MyungCollege of Pharmacy and Institute of Drug Research and Development, Chungnam National University, Daejeon, 34134, South Korea.
Kyung-Sun HeoCollege of Pharmacy and Institute of Drug Research and Development, Chungnam National University, Daejeon, 34134, South Korea. kheo@cnu.ac.kr.ORCID http://orcid.org/0000-0003-3800-7665
Chungnam National University · KR

Funding

National Research Foundation of Korea 2022R1A2C4001776National Research Foundation of Korea KNRF-2019R1C1C1007331
6 · The paper itself

Abstract

Disruption of the endothelial barrier function and reduction in cell migration leads to endothelial dysfunction. One of the most abundant human milk oligosaccharides, 6'-sialylactose (6'-SL), is reported to exert various biological functions related to inflammatory responses. In this study, we evaluated the effects of 6'-SL on lipopolysaccharide (LPS)-induced inflammation caused by endothelial barrier damage. Our results showed that LPS at 500 ng/mL strongly not only abolished cell migration but also hyperactivated MAPK and NF-κB pathways. 6'-SL suppressed LPS-induced endothelial inflammation via ERK1/2, p38, and JNK MAPK pathways. 6'-SL supported endothelial junctions by upregulating PECAM-1 expression and mRNA levels of tight junctions, such as ZO-1 and occludin, which were downregulated by LPS stimulation. It significantly inhibited the nuclear translocation of NF-κB, along with the downregulation of inflammatory cytokines, including TNF-α, IL-1β, MCP-1, VCAM-1, and ICAM-1. Furthermore, 6'-SL abolished NF-κB-mediated STAT3 in controlling endothelial migration and hyperpermeability via downregulating STAT3 activation and nuclear translocation. Finally, LPS induced over-expression of VCAM-1 and ZO-1 disassembly in both atheroprone and atheroprotective areas of mouse aorta, which were reversed by 6'-SL treatment. Altogether, our findings suggest that 6'-SL is a potent therapeutic agent for modulating inflammatory responses and endothelial hyperpermeability.

Indexed as

Endothelial CellsLipopolysaccharidesAnimalsHumansInflammationMiceNF-kappa BPermeabilityVascular Cell Adhesion Molecule-1LipopolysaccharidesNF-kappa BVascular Cell Adhesion Molecule-16′-SialyllactoseEndothelial hyperpermeabilityInflammatory responsesLipopolysaccharideNF-κBSTAT3

Identifiers

PMID36401777
OpenAlexW4309408852

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.