Evidence map›Paper›PMID 28260081›Full record

ArticleInternational journal of molecular medicine2017

Minocycline attenuates sevoflurane-induced cell injury via activation of Nrf2.

Yue Tian, Xiuying Wu, Shanbin Guo, Ling Ma, Wei Huang, Xiaochun Zhao

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2017. 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
1.4field-weighted citation impact, top 23% 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, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Cancer therapy and cachexia.The Journal of clinical investigation · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. 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

6 authors at 1 institution in 1 country.

Yue TianDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Xiuying WuDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Shanbin GuoDepartment of Pharmacy, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Ling MaDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Wei HuangDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Xiaochun ZhaoDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Minocycline has been demonstrated to exert neuroprotective effects in various experimental models. In the present study, we investigated the mechanisms underlying the protective effects of minocycline on cell injury induced by the inhalation of the anesthetic, sevoflurane. In our in vivo experiments using rats, minocycline attenuated sevoflurane-induced neuronal degeneration and apoptosis in the rat hippocampus, and this effect was associated with the minocycline-mediated suppression of oxidative stress in the hippocampus. In in vitro experiments, minocycline inhibited sevoflurane-induced apoptosis and the production of reactive oxygen species (ROS) in H4 human neuroglioma cells. In addition, minocycline suppressed the sevoflurane-induced upregulation of interleukin (IL)-6 and the activation of the nuclear factor-κB (NF-κB) signaling pathway in H4 cells. Furthermore, we found that nuclear factor E2-related factor 2 (Nrf2), an activator of the stress response, was upregulated and activated upon sevoflurane treatment both in the rat hippocampus and in H4 cells. In addition, minocycline further augmented the upregulation and activation of Nrf2 when used in conjunction with sevoflurane. Moreover, the knockdown of Nrf2 in H4 cells by small interfering RNA (siRNA) diminished the cytoprotective effect of minocycline, and attenuated the inhibitory effect of minocycline on ROS production, IL-6 upregulation and the activation of the NF-κB signaling pathway. On the whole, our findings indicate that minocycline may exert protective effects against sevoflurane-induced cell injury via the Nrf2-modulated antioxidant response and the inhibition of the activation of the NF-κB signaling pathway.

Indexed as

HippocampusAnimalsCell Line, TumorInterleukin-6MaleMethyl EthersMinocyclineNF-E2-Related Factor 2NF-kappa BRatsRats, Sprague-DawleyReactive Oxygen SpeciesSevofluraneSignal TransductionInterleukin-6Methyl EthersMinocyclineNfe2l2 protein, ratNF-E2-Related Factor 2NF-kappa BReactive Oxygen SpeciesSevoflurane

Identifiers

PMID28260081
PMCPMC5360434
OpenAlexW2593357086

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.