Evidence map›Paper›PMID 32293462›Full record

ArticleJournal of translational medicine2020

HSP90 inhibitor 17AAG attenuates sevoflurane-induced neurotoxicity in rats and human neuroglioma cells via induction of HSP70.

Min Liu, Moyun Li, Yu Zhou, Qian Zhou, Yugang Jiang

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. [Geniposide inhibits retinal cell apoptosis induced by glaucoma through the Hspa1a pathway].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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

5 authors at 2 institutions in 1 country.

Min LiuDepartment of Neurosurgery, The Second Xiangya Hospital of Central South University, No. 139, Changsha City, 410000, Hunan Province, People's Republic of China.
Moyun LiDepartment of General Surgery, The Second Xiangya Hospital of Central South University, Changsha City, 410000, Hunan Province, People's Republic of China.
Yu ZhouDepartment of Neurosurgery, The Second Xiangya Hospital of Central South University, No. 139, Changsha City, 410000, Hunan Province, People's Republic of China.
Qian ZhouDepartment of Neurosurgery, The Second Xiangya Hospital of Central South University, No. 139, Changsha City, 410000, Hunan Province, People's Republic of China.
Yugang JiangDepartment of Neurosurgery, The Second Xiangya Hospital of Central South University, No. 139, Changsha City, 410000, Hunan Province, People's Republic of China. xy16liumin@csu.edu.cn.
Second Xiangya Hospital of Central South University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background17AAG has been extensively studied for its antitumor effects that protect cells from lethal stress by maintaining protein stability. The role of 17AAG in sevoflurane-induced neuronal injury has never been studied. We aim to investigate the effect of 17AAG on sevoflurane-induced neurotoxicity in vivo and in vitro.

methodsSevoflurane-induced hippocampal neuron injury model was established in aged Sprague-Dawley rats. Pretreatment of vehicle or 17AAG was administered prior to sevoflurane inhalation. H4 neuroglioma cells were pretreated with vehicle or 17AAG and exposed to sevoflurane. Apoptosis, oxidative stress, expression of interleukin-6 (IL-6), and activation of the nuclear factor-κB (NF-κB) signaling pathway in H4 cells were examined by Hoechst assay, flow cytometry, Western blot, and immunofluorescent staining. RNA interference against HSPA1A was performed to test the function of HSP70 in neuroprotection.

resultsExogenous 17AAG reduced sevoflurane-induced apoptosis and oxidative stress in rat hippocampal neurons and in H4 cells. In H4 cells, 17AAG suppressed sevoflurane-induced upregulation of IL-6 and activation of NF-κB signaling. 17AAG enhanced sevoflurane-induced upregulation of HSP70 in rat hippocampal neurons and in H4 cells. Conversely, silencing of HSPA1A in H4 cells blocked the cytoprotective effect of 17AAG against sevoflurane-induced apoptosis and oxidative stress, and prevented upregulation of IL-6 and activation of NF-κB signaling.

conclusions17AAG protects against sevoflurane-induced neurotoxicity in vivo and in vitro via HSP70-dependent inhibition of apoptosis, oxidative stress, and pro-inflammatory signaling pathway.

Indexed as

ApoptosisBenzoquinonesAnimalsHumansLactams, MacrocyclicNF-kappa BRatsRats, Sprague-DawleySevofluraneBenzoquinonesLactams, MacrocyclicNF-kappa BSevofluranetanespimycin17-N-allylamino-17-demethoxygeldanamycin (17AAG)Anesthetic neurotoxicityApoptosisHeat shock proteinNF-κBOxidative stress

Identifiers

PMID32293462
PMCPMC7158111
OpenAlexW3016042550

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.