Evidence map›Paper›PMID 39165322›Full record

ArticleJournal of inflammation research2024

Bitongqing Attenuates CIA Rats by Suppressing Macrophage Pyroptosis and Modulating the NLRP3/Caspase-1/GSDMD Pathway.

Yunxia Wu, Yue Zhang, Zishan Wang, Yun Lu, Yabei Wang, Jie Pan, Chenxi Liu, Wen Zhu, Yue Wang

Abstract read
In one paragraph

Article in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. The "Tianyu" Formulation Alleviates Rheumatoid Arthritis by Modulating the NLRP3/Caspase-1/GSDMD-Mediated Pyroptosis Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. 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

9 authors.

Yunxia Wu *Academy of First Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People's Republic of China.ORCID 0009-0009-7181-5497
Yue Zhang *Academy of First Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People's Republic of China.
Zishan WangAcademy of First Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People's Republic of China.
Yun LuAcademy of First Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People's Republic of China.
Yabei WangAcademy of First Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People's Republic of China.
Jie PanAcademy of First Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People's Republic of China.
Chenxi LiuAcademy of First Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People's Republic of China.
Wen Zhu *Department of Rheumatology & Immunology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People's Republic of China.
Yue Wang *Department of Rheumatology & Immunology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovitis and inflammatory cell infiltration. The traditional Chinese medicine prescription, Bitongqing (BTQ) exhibited significant efficacy in the clinical treatment of RA. However, the potential therapeutic mechanisms of BTQ in treating RA have not been fully investigated. This study aims to elucidate the effect of BTQ on collagen-induced arthritis (CIA) rat macrophage pyroptosis, providing a theoretical basis for treating RA. Methods: This research employed liquid chromatography-mass spectrometry (LC-MS) to identify the primary components of BTQ. The therapeutic effects of BTQ were evaluated in a rat model of CIA. In vivo experiments were conducted using pathohistological staining, immunofluorescence, micro-CT, and Western blotting. Next, Mouse leukemia cells of monocyte macrophage cells (RAW264.7) were induced to undergo pyroptosis using lipopolysaccharide (LPS) and adenosine triphosphate (ATP), and the impact of BTQ on RAW264.7 macrophages was assessed through cell viability, immunofluorescence analysis, lactate dehydrogenase (LDH) secretion measurement, and Western blotting. Results: BTQ had a therapeutic effect on CIA rats, which was mainly manifested as a reduction in joint inflammation, foot swelling, bone erosion, and amelioration of pathological changes in these rats. Further studies revealed that BTQ inhibited the levels of cytokine production interleukin-18 (IL-18) and interleukin-1β (IL-1β), and likewise, it inhibited the expression of key proteins in the NOD-like receptor thermal protein domain associated protein 3 (NLRP3) mediated pyroptosis in the synovial tissues of CIA rats. The results of in vitro experiments demonstrated that BTQ attenuated LDH secretion, decreased IL-18 and IL-1β cytokine production, and downregulated expression of key proteins involved in the NLRP3-mediated pyroptosis on RAW264.7 macrophages. Conclusion: The therapeutic potential of BTQ in CIA lies in its ability to inhibit NLRP3-mediated macrophage pyroptosis, thereby suggesting a promising strategy for the treatment of RA.

Indexed as

BitongqingmacrophageNLRP3 inflammasomepyroptosisrheumatoid arthritis

Identifiers

PMID39165322
PMCPMC11335010

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