Evidence map›Paper›PMID 26770373›Full record

ArticleInternational journal of clinical and experimental medicine2015

Sulforaphane exerts neuroprotective effects via suppression of the inflammatory response in a rat model of focal cerebral ischemia.

Li-Li Ma, Guo-Ping Xing, Yin Yu, Hui Liang, Tian-Xia Yu, Wei-Hong Zheng, Tian-Bao Lai

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. The Nrf2 Pathway in Ischemic Stroke: A Review.Molecules (Basel, Switzerland) · 2021
    Review
  6. The Role of Supplementation with Natural Compounds in Post-Stroke Patients.International journal of molecular sciences · 2021
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
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

7 authors at 4 institutions in 1 country.

Li-Li MaDepartment of Neurology, Yantaishan Hospital Yantai 264000, China.
Guo-Ping XingDepartment of Neurology, Weifang People's Hospital Weifang 261599, China.
Yin YuDepartment of Neurosurgery, The Third Hospital (China-Japan Union Hospital) of Jilin University Changchun 130033, China.
Hui LiangDepartment of Neurology, Yantaishan Hospital Yantai 264000, China.
Tian-Xia YuDepartment of Neurology, Yantaishan Hospital Yantai 264000, China.
Wei-Hong ZhengDepartment of Neurology, Zhongshan Hospital, Xiamen University Xiamen 361004, China.
Tian-Bao LaiDepartment of Neurology, Zhongshan Hospital, Xiamen University Xiamen 361004, China.
Yantaishan Hospital · CNZhongshan Hospital of Xiamen University · CNUnion Hospital · CNWeifang People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory damage plays an important role in cerebral ischemic pathogenesis and may represent a promising target for treatment. Sulforaphane exerts protective effects in a rat model of focal cerebral ischemia/reperfusion injury by alleviating brain edema. However, the possible mechanisms of sulforaphane after cerebral ischemia/reperfusion injury have not been fully elucidated. Therefore, in the present study, we investigated the effect of sulforaphane on inflammatory reaction and the potential molecular mechanisms in cerebral ischemia rats. We found that sulforaphane significantly attenuated the blood-brain barrier (BBB) disruption; decreased the levels of pro-inflammatory cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-1β; reduced the nitric oxide (NO) levels and inducible nitric oxide synthase (iNOS) activity; inhibited the expression of iNOS and cyclooxygenase-2 (COX-2). In addition, sulforaphane inhibits the expression of p-NF-κB p65 after focal cerebral ischemia-reperfusion injury. Taken together, our results suggest that sulforaphane suppresses the inflammatory response via inhibiting the NF-κB signaling pathway in a rat model of focal cerebral ischemia, and sulforaphane may be a potential therapeutic agent for the treatment of cerebral ischemia injury.

Indexed as

focal cerebral ischemiainflammatory responseSulforaphane

Identifiers

PMID26770373
PMCPMC4694273
OpenAlexW2403889823

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.