Evidence map›Paper›PMID 35931839›Full record

ArticleInflammation2022

Pectolinarigenin Suppresses LPS-Induced Inflammatory Response in Macrophages and Attenuates DSS-Induced Colitis by Modulating the NF-κB/Nrf2 Signaling Pathway.

Yuling Feng, Ramesh Bhandari, Chunmeng Li, Pengfei Shu, Imran Ibrahim Shaikh

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. IL-1βJournal of neuroinflammation · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Pectolinarigenin ameliorated airway inflammation and airway remodeling to exhibit antitussive effect.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. 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

5 authors at 2 institutions in 1 country.

Yuling Feng *Department of Vascular Surgery, Lishui People's Hospital, The Sixth Affiliated Hospital of Wenzhou Medical University, Lishui, Zhejiang, 323000, China.
Ramesh Bhandari *Department of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.
Chunmeng LiDepartment of Vascular Surgery, Wenzhou Medical University, Wenzhou Central Hospital, 252 Baili East Road, Lucheng District, Wenzhou, Zhejiang, 325000, China.
Pengfei ShuDepartment of Vascular Surgery, Lishui People's Hospital, The Sixth Affiliated Hospital of Wenzhou Medical University, Lishui, Zhejiang, 323000, China.
Imran Ibrahim Shaikh *Department of Orthopedics, Tongji Hospital, School of Medicine, Tongji University, 389 Xincun Road, Shanghai, 200065, China. imranshaikh88@tongji.edu.cn.ORCID http://orcid.org/0000-0002-3083-3025
Wenzhou Medical University · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pectolinarigenin (PEC), a natural flavonoid present in cirsium chanroenicum and citrus fruits, has possess the distinct pharmacological activities. However, its molecular mechanisms and pharmacological effects on intestinal illness have not been elucidated. In the present study, we investigated the potential beneficial effects of pectolinarigenin (PEC) on lipopolysaccharide (LPS)-induced macrophage cells and the dextran sulfate sodium (DSS)-induced colitis model. Our findings showed that PEC pretreatment inhibits the LPS-induced nuclear factor-kappa B (NF-κB) activation by interfering with the degradation of IκB-α. Further, increased Nrf2 protein expression was reported on PEC treated RAW 264.7 and THP1 cell lines. In addition, we revealed that PEC mediated the NF-κB/Nrf2 pathway regulation, which in turn inhibits the synthesis of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), interleukin-1beta (IL-1β), and tumor necrosis factor-alpha (TNF-α) on RAW 264.7 and THP1 cells. Furthermore, PEC dose-dependently reduced the DSS-induced inflammation in the colon by regulating NF-κB/Nrf2 signaling pathway and enhancing the myeloperoxidase (MPO) activity and redox regulators such as superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and lipid peroxidation byproduct malondialdehyde (MDA) in DSS-induced inflamed colon. Similarly, we reported the minimal pathological damages in the PEC-treated mice colon, as well as increase goblet cell population and mucin-2 production. In conclusion, our findings demonstrate that PEC reduces the DSS-induced colitis in mice by regulating the NF-κB/Nrf2 pathway. Thus, PEC might be a promising therapeutic agent for the treatment of inflammatory bowel disease.

Indexed as

ColitisNF-kappa BAnimalsChromonesDextran SulfateLipopolysaccharidesMacrophagesMiceNF-E2-Related Factor 2Signal TransductionChromonesDextran SulfateLipopolysaccharidesNF-E2-Related Factor 2NF-kappa BpectolinarigeninAntioxidantDextran sulfate sodiumGoblet cellsNuclear factor-kappa BPectolinarigenin

Identifiers

PMID35931839
OpenAlexW4290048190

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.