Evidence map›Paper›PMID 27413257›Full record

ArticleMediators of inflammation2016

Triptolide Inhibits Osteoclast Differentiation and Bone Resorption In Vitro via Enhancing the Production of IL-10 and TGF-β1 by Regulatory T Cells.

Huihui Xu, Hongyan Zhao, Cheng Lu, Qi Qiu, Gui Wang, Jing Huang, Minghui Guo, Baosheng Guo, Yong Tan, Cheng Xiao

Abstract read
In one paragraph

Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
–field-weighted citation impact
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

35 citing papers in PubMed.

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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

10 authors.

Huihui XuBeijing University of Chinese Medicine, Beijing 100029, China; Institute of Clinical Medicine, China-Japan Friendship Hospital, Beijing 100029, China.
Hongyan ZhaoInstitute of Basic Theory of Chinese Medicine, China Academy of Chinese Medical Science, Beijing 100700, China.
Cheng LuInstitute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Science, Beijing 100700, China.ORCID 0000-0002-6474-9198
Qi QiuInstitute of Clinical Pharmacology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.ORCID 0000-0001-7756-7134
Gui WangBeijing University of Chinese Medicine, Beijing 100029, China; Institute of Clinical Medicine, China-Japan Friendship Hospital, Beijing 100029, China.
Jing HuangBeijing University of Chinese Medicine, Beijing 100029, China; Institute of Clinical Medicine, China-Japan Friendship Hospital, Beijing 100029, China.
Minghui GuoBeijing University of Chinese Medicine, Beijing 100029, China; Institute of Clinical Medicine, China-Japan Friendship Hospital, Beijing 100029, China.
Baosheng GuoInstitute for Advancing Translational Medicine in Bone & Joint Diseases, School of Chinese Medicine, Hong Kong Baptist University, Kowloon Tong, Hong Kong.
Yong TanInstitute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Science, Beijing 100700, China.
Cheng XiaoInstitute of Clinical Medicine, China-Japan Friendship Hospital, Beijing 100029, China.ORCID 0000-0002-5601-9670

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triptolide, a purified component of Tripterygiumwilfordii Hook F, has been shown to have immunosuppressive and anti-inflammatory properties in rheumatoid arthritis (RA). Although triptolide has demonstrated that it could suppress bone destruction in collagen-induced mice, its therapeutic mechanism remains unclear. Many studies have investigated the effect of triptolide on Tregs and Tregs-related cytokine involved in RA. Additionally, previous studies have implied that Tregs inhibit osteoclast differentiation and bone resorption. Thus, in this study we aimed to explore the regulatory mechanism by which triptolide influences the Treg-mediated production of IL-10 and TGF-β1 to affect osteoclast differentiation and bone resorption. In cocultures system of Tregs and mouse bone marrow macrophages (BMMs), Tregs inhibited the differentiation of osteoclasts and reduced the resorbed areas significantly and the production of both IL-10 and TGF-β1 was upregulated. When the coculture systems were pretreated with triptolide, they produced higher levels of IL-10 and TGF-β1. Our data indicate that triptolide enhances the suppressive effects of Tregs on osteoclast differentiation and bone resorption by enhancing the secretion of IL-10 and TGF-β1. Tregs are most likely involved in the triptolide-mediated regulation of bone metabolism and may provide a potential therapeutic target for the treatment of inflammatory bone destruction.

Indexed as

AnimalsAnti-Inflammatory AgentsBone Marrow CellsBone ResorptionCell DifferentiationCoculture TechniquesCollagenDiterpenesEpoxy CompoundsImmunosuppressive AgentsInterleukin-10Interleukin-2 Receptor alpha SubunitMacrophagesMaleMiceMice, Inbred C57BLAnti-Inflammatory AgentsCollagenDiterpenesEpoxy CompoundsIL10 protein, mouseIl2ra protein, mouseImmunosuppressive AgentsInterleukin-10Interleukin-2 Receptor alpha SubunitPhenanthrenesTartrate-Resistant Acid PhosphataseTgfb1 protein, mouseTransforming Growth Factor beta1triptolide

Identifiers

PMID27413257
PMCPMC4930824

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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.