Evidence map›Paper›PMID 33222058›Full record

ArticleNeurochemical research2021

N-acetylserotonin Derivative Exerts a Neuroprotective Effect by Inhibiting the NLRP3 Inflammasome and Activating the PI3K/Akt/Nrf2 Pathway in the Model of Hypoxic-Ischemic Brain Damage.

Xing Luo, Honglan Zeng, Chengzhi Fang, Bing-Hong Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2021. 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
1.8field-weighted citation impact, top 14% 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, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Drug Design for Cerebral Ischemia: A Molecular Perspective Review.CNS & neurological disorders drug targets · 2026
    Review
  4. Article
  5. NLRP3 inflammasome: a key player in neonatal brain injury.Clinical and experimental pediatrics · 2025
    Article
  6. Review
  7. Article
  8. N-acetylserotonin alleviates retinal ischemia-reperfusion injuryInternational journal of ophthalmology · 2024
    Article
  9. Article
  10. Article
  11. A key role for NLRP3 signaling in preterm labor and birth driven by the alarmin S100B.Translational research : the journal of laboratory and clinical medicine · 2023
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  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

4 authors at 1 institution in 1 country.

Xing LuoDepartments of Neonatology, Renmin Hospital of Wuhan University, Ziyang Road Wuchang District, No. 99 Jiefang Road, Wuhan, 430060, Hubei Province, China.
Honglan ZengDepartments of Neonatology, Renmin Hospital of Wuhan University, Ziyang Road Wuchang District, No. 99 Jiefang Road, Wuhan, 430060, Hubei Province, China.
Chengzhi FangDepartments of Neonatology, Renmin Hospital of Wuhan University, Ziyang Road Wuchang District, No. 99 Jiefang Road, Wuhan, 430060, Hubei Province, China. fcz2000@126.com.
Bing-Hong ZhangDepartments of Neonatology, Renmin Hospital of Wuhan University, Ziyang Road Wuchang District, No. 99 Jiefang Road, Wuhan, 430060, Hubei Province, China. zbhong6288@163.com.ORCID http://orcid.org/0000-0002-3118-3917
Wuhan University · CN

Funding

Natural Science Foundation of Hubei Province WJ2019M184the Central Fund for Guiding Local Science and Technology Development No.[2016]109
6 · The paper itself

Abstract

Neonatal hypoxic-ischemic encephalopathy (HIE) is one of the main causes of neonatal disability and death. As a derivative of N-acetylserotonin, N-[2-(5-hydroxy-1H-indol-3-yl) ethyl]-2-oxopiperidine-3-carboxamide (HIOC) can easily cross the blood-brain barrier and have a long half-life in the brain. In this study, the hypothesis was verified that HIOC plays a neuroprotective role in the HIE model and its potential mechanism was evaluated. Firstly, an HIE rat model was established to deliver HIOC, revealing that it can reduce cerebral infarction volume, cerebral edema, and neuronal apoptosis. The results of immunofluorescence staining, Western blots and RT-PCR further showed that HIOC could inhibit the activation of the NLRP3 inflammasome and the expression of related proteins. Finally, the activation of the phosphatidylinositol-3-kinase (PI3K)/Akt/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway by HIOC was verified in vitro and in vivo. It was discovered that HIOC could increase the nuclear translocation of Nrf2, and that this induction can be reversed by the PI3K/Akt pathway inhibitor LY294002. In general terms, the neuroprotective effect of HIOC was confirmed in the HIE model, which is related to the activation of the Pi3k/Akt/Nrf2 signal pathway and the inhibition of the NLRP3 inflammasome.

Indexed as

Hypoxia-Ischemia, BrainInflammasomesNeuroprotective AgentsNLR Family, Pyrin Domain-Containing 3 ProteinSerotoninSignal TransductionAnimalsApoptosisCerebral CortexHippocampusNeuronsNF-E2-Related Factor 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyInflammasomesN-acetylserotoninNeuroprotective AgentsNF-E2-Related Factor 2NLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSerotoninHypoxic-ischemic encephalopathyN-[2-(5-hydroxy-1H-indol-3-yl) ethyl]-2-oxopiperidine-3-carboxamideNLRP3 inflammasomeNrf2

Identifiers

PMID33222058
OpenAlexW3108567237

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.