Evidence map›Paper›PMID 31897915›Full record

ArticleInflammation2020

Sevoflurane Post-treatment Upregulated miR-203 Expression to Attenuate Cerebral Ischemia-Reperfusion-Induced Neuroinflammation by Targeting MyD88.

Huagen Zhong, Hui Chen, Changwei Gu

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.8field-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

18 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The Role of microRNA in Anaesthetics-induced Brain Injury: A Narrative Review.Turkish journal of anaesthesiology and reanimation · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. 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

3 authors at 2 institutions in 1 country.

Huagen ZhongDepartment of Anesthesiology, Taizhou Hospital of Traditional Chinese Medicine, Taizhou City, 225300, Jiangsu Province, China.
Hui ChenDepartment of Neurology, Affilicated Jinan Third Hospital of Jining Medical University, Jinan City, 250132, Shandong Province, China.
Changwei GuEmergency Department, The Second Affiliated Hospital of Xi'an Jiaotong University, No. 157, Xiwu Road, Xincheng District, Xi'an City, 710004, Shaanxi Province, China. fgmezgqg@163.com.ORCID http://orcid.org/0000-0002-5977-0275
Fourth People’s Hospital of Jinan · CNSecond Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To investigate the expression of miR-203 by sevoflurane treatment and its effect on neuroinflammation induced by cerebral ischemia-reperfusion. Rats were randomly divided into sham operation group (C), cerebral ischemia-reperfusion group (I/R), and sevoflurane treatment group (S). The neurological function score was evaluated. The area of cerebral infarction was evaluated by TTC staining. The expression of inflammatory factor in brain tissue was detected by ELISA. The apoptosis of neurons was detected by TUNEL. A miR-203 agonist and inhibitor treated the cerebral ischemia-reperfusion model. The luciferase assay verified whether miR-203 targeted MyD88. To further verify the relationship between miR-203 and MyD88, the I/R group was treated with MyD88 activator and inhibitor, and the mRNA expressions of miR-203 and MyD88 in brain tissue were detected by RT-PCR. Western blot was used to detect the expression of MyD88 protein in brain tissue, and the above experiment was repeated. Compared with the I/R group, miR-203 mRNA was significantly increased in brain tissue and the neurological function score, the area of cerebral infarction, the expression of inflammatory factor, and MyD88 mRNA were decreased in the S group (P < 0.05). After treatment of miR-203 agonist and inhibitor in the I/R group, overexpression of miR-203 could alleviate cerebral ischemia-reperfusion injury, and miR-203 inhibitor could aggravate cerebral ischemia-reperfusion injury. The miR-203 agonist could enhance the action of sevoflurane, and the miR-203 inhibitor could reverse the action of sevoflurane. miR-203 agonist treatment could inhibit the expression of MyD88 gene and protein and reduce the neuroinflammation induced by cerebral ischemia-reperfusion. The treatment of sevoflurane upregulated miR-203 expression, which targeted MyD88 and attenuate neuroinflammation induced by cerebral ischemia-reperfusion.

Indexed as

AnimalsBrain IschemiaDrug Delivery SystemsGene ExpressionInflammationMaleMicroRNAsMyeloid Differentiation Factor 88Platelet Aggregation InhibitorsRandom AllocationRatsRats, Sprague-DawleyReperfusion InjurySevofluraneUp-RegulationMicroRNAsMIRN203 microRNA, ratMyd88 protein, ratMyeloid Differentiation Factor 88Platelet Aggregation InhibitorsSevofluranecerebral ischemia-reperfusionmiR-203neuroinflammationsevoflurane

Identifiers

PMID31897915
OpenAlexW2997979546

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.