Evidence map›Paper›PMID 30944203›Full record

ArticleBioscience reports2019

Fluoxetine suppresses inflammatory reaction in microglia under OGD/R challenge via modulation of NF-κB signaling.

Mouli Tian, Mei Yang, Zhenjie Li, Yiru Wang, Wei Chen, Liye Yang, Yonghua Li, Hongbin Yuan

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Mouli TianDepartment of Anesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Mei YangDepartment of Anesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Zhenjie LiDepartment of Anesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Yiru WangDepartment of Anesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Wei ChenDepartment of Anesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Liye YangDepartment of Anesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Yonghua LiDepartment of Anesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai, China jfjczyy@aliyun.com liyonghua1207@126.com.
Hongbin YuanDepartment of Anesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai, China jfjczyy@aliyun.com liyonghua1207@126.com.ORCID 0000-0001-8468-4005
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We aimed to investigate the anti-inflammatory role of fluoxetine, a selective serotonin reuptake inhibitor, in microglia (MG) and the mechanisms under oxygen glucose deprivation/reoxygenation (OGD/R). An OGD/R model on BV-2 cells was used for the study of microglia under ischemia/reperfusion injury in ischemic stroke. Lentiviral transfection was applied to knock down IκB-α. Enzyme-linked immunosorbent assay (ELISA) was used for detecting levels of TNF-α, IL-1β, and IL-6, and real-time PCR was used to assess the expression of IκB-α protein. Western blotting was applied to analyze NF-κB-signaling related proteins and Cell Counting Kit-8 (CCK-8) was used for assessing cell viability. Molecular docking and drug affinity responsive target stability (DARTS) assay were used for the detection of the interaction between IκB-α and fluoxetine. We found that fluoxetine decreased the levels of TNF-α, IL-1β, and IL-6 in supernatant as well as NF-κB subunits p65 and p50 in BV-2 cells under OGD/R. Fluoxetine significantly increased the level of IκB-α through the inhibition of IκB-α ubiquitylation and promoted the bonding of IκB-α and fluoxetine in BV-2 cells under OGD/R. Knocking down IκB-α attenuated the decreasing effect of TNF-α, IL-1β, and IL-6 as well as p65 and p50 in BV-2 cells under OGD/R led to by fluoxetine. In conclusion, our present study demonstrated the anti-inflammatory role of fluoxetine and its mechanisms related to the modulation of NF-κB-related signaling in MG under ischemia/reperfusion challenge.

Indexed as

AnimalsApoptosisFluoxetineGene Expression RegulationGlucoseHumansInflammationInterleukin-1betaInterleukin-6MiceMicrogliaMolecular Docking SimulationNF-kappa BNF-KappaB Inhibitor alphaOxygenReperfusion InjuryFluoxetineGlucoseIL1B protein, mouseInterleukin-1betaInterleukin-6NF-kappa BNF-KappaB Inhibitor alphaOxygenSelective Serotonin Reuptake InhibitorsTranscription Factor RelATumor Necrosis Factor-alphafluoxetineinflammationmicrogliaNF-κBOGD/R

Identifiers

PMID30944203
PMCPMC6487262
OpenAlexW2935132071

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.