Evidence map›Paper›PMID 32103436›Full record

ArticleInflammation2020

N-Acetylcysteine Attenuates Lipopolysaccharide-Induced Osteolysis by Restoring Bone Remodeling Balance via Reduction of Reactive Oxygen Species Formation During Osteoclastogenesis.

Guangqi Yan, Yan Guo, Jingwen Guo, Qiang Wang, Chunyu Wang, Xue Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2020. 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
1.1field-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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. [Preparation of B@PH/GM-V hydrogel microspheres and their antioxidant and osteogenesis-promoting effects].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2026
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  15. Recent Advances in Zinc Oxide Nanostructures with Antimicrobial Activities.International journal of molecular sciences · 2020
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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

6 authors at 2 institutions in 1 country.

Guangqi YanDepartment of Oral and Maxillofacial Surgery, School of Stomatology, China Medical University, Shenyang, 110002, Liaoning, China.
Yan GuoKey Laboratory of Oral Disease Liaoning Province, Shenyang, 110002, Liaoning, China.
Jingwen GuoDepartment of Pharmacy, The First Affiliated Hospital of China Medical University, Shenyang, 110016, Liaoning, China.
Qiang WangDepartment of Central Laboratory, School of Stomatology, China Medical University, Shenyang, 110002, Liaoning, China.
Chunyu WangDepartment of Cell Biology, Key Laboratory of Cell Biology, and Key Laboratory of Medical Cell Biology, School of Life Sciences, China Medical University, Shenyang, 110122, Liaoning, China.
Xue WangDepartment of Orthodontics, School of Stomatology, China Medical University, 117# Nanjingbei Street, Shenyang, 110002, Liaoning, China. wang666666xue@163.com.ORCID http://orcid.org/0000-0003-0785-7376
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

Natural foundation planned project of Liaoning Province 2019-ZD-0793Supported project for young technological innovation-talents in Shenyang NO. RC170541
6 · The paper itself

Abstract

Chronic inflammatory diseases affect bone and teeth health tremendously. Characterized by osteolytic lesion and hyperactive osteoclastogenesis, inflammatory bone diseases are short of effective therapeutics and therefore highlight the importance of understanding pathogenesis and developing ideal medications. Reactive oxygen species (ROS) play a prominent role in the innate immune response of activated macrophages, as well as in the physiological signaling of osteoclasts (OCs) differentiation. N-acetylcysteine (NAC) is a potent ROS scavenger and a potential option for treating diseases characterized by excessive ROS generation. However, whether NAC can protect physiological bone remodeling from in vivo inflammatory conditions is largely undefined. We applied NAC treatment on lipopolysaccharide (LPS)-induced inflammatory osteolysis mice model and found that NAC could attenuate bone erosion and protect mice against LPS-induced osteolysis, due to the suppressive effect on osteoclastogenesis and stimulated effect on osteogenesis. Moreover, in vitro study demonstrated that, in OC precursors (pre-OCs), LPS-stimulated expressions of OC marker genes, such as tartrate-resistant acid phosphatase type 5 (Acp5), cathepsin K (Ctsk), OC stimulatory transmembrane protein (Oc-stamp), dendritic cell-specific transmembrane protein (Dc-stamp), and nuclear factor of activated T cells 1 (NFATc1), were all reduced because of the NAC pretreatment, thereby adversely affecting OC function including F-actin ring formation and bone resorption. Further mechanism study showed that NAC blocked LPS-induced ROS formation in both macrophages and pre-OCs, cutting off the LPS-stimulated autocrine/paracrine mechanism during inflammatory osteolysis. Our findings reveal that NAC attenuates inflammatory osteolysis via the elimination of ROS formation during LPS-stimulated osteoclastogenesis, and provide a potential therapeutic approach to treat inflammatory bone disease.

Indexed as

AcetylcysteineAnimalsBone RemodelingCells, CulturedFemaleFree Radical ScavengersLipopolysaccharidesMaleMiceMice, Inbred C57BLOsteoclastsOsteogenesisOsteolysisReactive Oxygen SpeciesAcetylcysteineFree Radical ScavengersLipopolysaccharidesReactive Oxygen Speciesinflammatory bone diseaseinflammatory osteolysisLPSN-acetylcysteine (NAC)osteoclastROS

Identifiers

PMID32103436
OpenAlexW3008889493

What OpenQuestion holds

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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.