Evidence map›Paper›PMID 26860538›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2016

Autophagy upregulation promotes macrophages to escape mesoporous silica nanoparticle (MSN)-induced NF-κB-dependent inflammation.

Chen Xi, Jie Zhou, Shuzhang Du, Shaojun Peng

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 47 citations in OpenAlex.

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  15. Particle toxicology and health - where are we?Particle and fibre toxicology · 2019
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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

4 authors at 2 institutions in 1 country.

Chen XiPharmaceutical Department, The First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, People's Republic of China.
Jie ZhouSchool of Medicine, Yichun University, 576 XueFu Road, Yuanzhou District, 336000, Yichun, People's Republic of China. zj9032@126.com.
Shuzhang DuPharmaceutical Department, The First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, People's Republic of China. du_shuzhang@126.com.
Shaojun PengSchool of Medicine, Yichun University, 576 XueFu Road, Yuanzhou District, 336000, Yichun, People's Republic of China.
First Affiliated Hospital of Zhengzhou University · CNYichun University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOur previous studies (Int J Nanomed 10:22, 2015) have indicated that a single large dose of mesoporous silica nanoparticles (MSNs) can induce severe and selective nephrotoxicity, which is closely related to inflammation mediated by the NF-κB pathway. However, the effect of MSNs on other organs and the interactions of nanomaterials with biological systems remain rudimentary.

objectiveThis study aimed to clarify the biological behaviour and influence of MSNs on macrophages.

methodsThe mice received a single intraperitoneal injection of a suspension of 150, 300 of 600 mg/kg MSNs, and RAW 264.7 cells were treated with MSNs at various concentrations and times. Cell viability was determined by MTT assay and LDH release assay. The NF-κB pathway and the target proinflammatory cytokines IL-1β and TNF-α were determined by western blotting or ELISA. Autophagy is considered as an emerging mechanism of nanomaterials. So the autophagic ultrastructural analysis, the determination of Beclin-1 and LC3 expression, and the calculation of LC3II dots were employed to verify autophagy activation. In addition, RNA interference, autophagy agonist and inhibitor were used to explore the role of autophagy in inflammation.

resultsThe results indicated that MSNs are internalized into macrophages and induce cytotoxicity in a dose- and time-dependent manner. The NF-κB pathway, IL-1β and TNF-α were induced and released by MSNs. The levels of Beclin-1 and LC3II dots were obviously up-regulated by MSNs, which indicated that autophagy was induced in the MSN-treated cells. Moreover, the enhanced autophagy can attenuate the inflammation mediated by the NF-κB pathway, whereas the inhibition of autophagy can contribute to inflammation.

conclusionsIn summary, our results suggest that autophagy may be a possible protective factor in inflammation induced by MSNs in macrophages.

Indexed as

AnimalsAutophagyCell LineCell SurvivalFemaleInflammationInterleukin-1betaLiverMacrophagesMice, Inbred BALB CMicroscopy, Electron, TransmissionNanoparticlesNF-kappa BPorositySilicon DioxideTumor Necrosis Factor-alphaInterleukin-1betaNF-kappa BSilicon DioxideTumor Necrosis Factor-alphaAutophagyInflammationMacrophageMesoporous silica nanoparticles (MSNs)NF-κB

Identifiers

PMID26860538
OpenAlexW2264498914

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.