Evidence map›Paper›PMID 32005962›Full record

ArticleScientific reports2020

Quzhou Fructus Aurantii Extract suppresses inflammation via regulation of MAPK, NF-κB, and AMPK signaling pathway.

Lili Li, Jiaoting Chen, Lin Lin, Guixuan Pan, Sheng Zhang, Hao Chen, Majuan Zhang, Yaoxian Xuan, Yin Wang, Zhenqiang You

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

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  20. Polarization of Microglia and Its Therapeutic Potential in Sepsis.International journal of molecular sciences · 2022
    Review
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

10 authors at 3 institutions in 1 country.

Lili LiZhejiang Academy of Medical Sciences, Hangzhou Medical College, Hangzhou, Zhejiang, China.
Jiaoting ChenZhejiang Academy of Medical Sciences, Hangzhou Medical College, Hangzhou, Zhejiang, China.
Lin LinZhejiang Academy of Medical Sciences, Hangzhou Medical College, Hangzhou, Zhejiang, China.
Guixuan PanZhejiang Academy of Medical Sciences, Hangzhou Medical College, Hangzhou, Zhejiang, China.
Sheng ZhangZhejiang Academy of Medical Sciences, Hangzhou Medical College, Hangzhou, Zhejiang, China.
Hao ChenZhejiang Academy of Medical Sciences, Hangzhou Medical College, Hangzhou, Zhejiang, China.
Majuan ZhangZhejiang Academy of Medical Sciences, Hangzhou Medical College, Hangzhou, Zhejiang, China.
Yaoxian XuanZhejiang Academy of Medical Sciences, Hangzhou Medical College, Hangzhou, Zhejiang, China.
Yin WangZhejiang Academy of Medical Sciences, Hangzhou Medical College, Hangzhou, Zhejiang, China. wy3333@163.com.
Zhenqiang YouZhejiang Academy of Medical Sciences, Hangzhou Medical College, Hangzhou, Zhejiang, China. youzhenqiang0817@163.com.
Zhejiang Academy of Medical Sciences · CNHangzhou Medical College · CNZhejiang University of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The anti-inflammatory activity of Quzhou Fructus Aurantii Extract (QFAE) has been reported recently. Thus, present study aims to explore the mechanism of anti-inflammation of QFAE in vitro and in vivo to develop a lung phylactic agent. The anti-inflammatory mechanism of QFAE in RAW 264.7 cells and acute lung injury (ALI) mice model was determined by cytokines analysis, histopathological examination, Western blot assay, immunofluorescence, and immunohistochemistry analysis. The results showed that QFAE restrained mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) signaling pathways in LPS-induced RAW 264.7 cells, whereas AMP-activated protein kinase (AMPK) signaling pathways were activated, as revealed by prominent attenuation of phosphorylation of ERK, JNK, p38, p65, IκBα, RSK and MSK, and overt enhancement of phosphorylation of ACC and AMPKα. The levels of pro-inflammatory cytokines TNF, IL-6, and IL-1β were suppressed, whereas the level of anti-inflammatory cytokine IL-10 increased after pretreatment with QFAE in vivo and in vitro. Moreover, QFAE prevented mice from LPS-provoked ALI, bases on alleviating neutrophils, and macrophages in bronchoalveolar lavage fluid (BALF) and mitigatingpulmonary histological alters, as well as hematological change. The MAPK and NF-κB signaling pathways in LPS-stimulated ALI mice were dampened by QFAE pretreatment, whereas AMPK signaling pathways were accelerated, as testify by significant restraint of phosphorylation of ERK, JNK, p38, p65, and IκBα, and distinct elevation of phosphorylation of ACC and AMPKα. The remarkable anti-inflammatory effect of QFAE is associated with the suppression of MAPK and NF-κB signaling pathways and the initiation of AMPK signaling pathway.

Indexed as

AMP-Activated Protein KinasesAnimalsBlotting, WesternChromatography, High Pressure LiquidCytokinesDrugs, Chinese HerbalInflammationInterleukin-1betaInterleukin-6MAP Kinase Signaling SystemMiceMice, Inbred ICRNF-kappa BRAW 264.7 CellsSignal TransductionTumor Necrosis Factor-alphaAMP-Activated Protein KinasesCytokinesDrugs, Chinese Herbalfructus aurantii immaturusInterleukin-1betaInterleukin-6NF-kappa BTumor Necrosis Factor-alpha

Identifiers

PMID32005962
PMCPMC6994495
OpenAlexW3004061483

What OpenQuestion holds

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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.