Evidence map›Paper›PMID 37946472›Full record

ArticleJournal of traditional Chinese medicine = Chung i tsa chih ying wen pan2023

Electroacupuncture stimulating Zusanli (ST36), Sanyinjiao (SP6) in mice with collagen-induced arthritis leads to adenosine A2A receptor-mediated alteration of p38α mitogen-activated protein kinase signaling and inhibition of osteoclastogenesis.

D U Zhongheng, Cong Wenjie, Tang Kejing, Zheng Qiqi, Song Zhiwei, Chen Yong, Yang Su, Zhang Chunwu, Y E Tianshen

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan, 2023. 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
0.2field-weighted citation impact, top 40% 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

4 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
  2. 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 at 1 institution in 1 country.

D U ZhonghengDepartment of Acupuncture, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Cong WenjieDepartment of Acupuncture, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Tang KejingDepartment of Acupuncture, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Zheng QiqiDepartment of Acupuncture, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Song ZhiweiDepartment of Acupuncture, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Chen YongDepartment of Acupuncture, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Yang SuZhejiang Provincial Key Laboratory of Aging and Neurological Disorder Research, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Zhang ChunwuDepartment of Traditional Chinese Orthopedics & Traumatology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Y E TianshenDepartment of Acupuncture, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Wenzhou Medical University · CN

Funding

Electroacupuncture of Mice with CIA Mitigate Joint Damage by the p38MAPK Pathway FHY2019021Electroacupuncture of Mice with CIA Mitigate Joint Damage by the p38MAPK Pathway Y20190198Mechanism of Adenosine A2A Receptor Modulate Electroacupuncture Inhibiting Osteoclast Formation in Mice with Collagen-Induced Arthritis 81674053Role of P38 MAPK Pathway in the Inhibition of CIA Osteoclast Differentiation by Electroacupuncture via Adenosine Pathway LY20H270015
6 · The paper itself

Abstract

objectiveTo observe the effect of electroacupuncture (EA) stimulating Zusanli (ST36), Sanyinjiao (SP6) on inhibition of osteoclastogenesis and the role of the adenosine A2A receptor (A2AR) and the p38α Mitogen-Activated Protein Kinase (MAPK) signaling pathway in mediating this effect.

methodsMice with collagen induced arthritis (CIA) received different treatments. Immunohistochemistry and western blotting were used to determine the levels of multiple signaling molecules in these joints [receptor activator of nuclear transcription factor-κB (NF-κB) ligand (RANKL), receptor activator of NF-κB (RANK), tumor necrosis factor receptor associated factor 6 (TRAF6), p38α, NF-κB, and nuclear factor of activated T cells C1 (NFATc1)]. Osteoclasts were identified using tartrate-resistant acid phosphatase (TRAP) staining.

resultsThe immunohistochemistry results indicated upregulation of p38α, NF-κB, and NFATc1 in the CIA-control and CIA-EA-SCH58261 groups, but reduced levels in the CIA-EA group. Western blotting indicated upregulation of RANKL, RANK, TRAF6, p38α, NF-κB, and NFATc1 in the CIA-control and CIA-EA-SCH58261 groups, but reduced expression in the CIA-EA group. Osteoclasts were more abundant in the CIA-control and CIA-EA-SCH58261 groups than in the CIA-EA group.

conclusionsEA treatment enhanced the A2AR activity and inhibited osteoclast formation by inhibition of RANKL, RANK, TRAF6, p38α, NF-κB, and NFATc1. SCH58261 reversed the effect of EA. These results suggest that EA regulated p38α-MAPK signaling by increasing A2AR activity, which inhibited osteoclastogenesis.

Indexed as

Arthritis, ExperimentalElectroacupunctureMitogen-Activated Protein Kinase 14AnimalsCell DifferentiationMiceNF-kappa BOsteogenesisRANK LigandReceptor, Adenosine A2ASignal TransductionTNF Receptor-Associated Factor 6Mitogen-Activated Protein Kinase 14NF-kappa BRANK LigandReceptor, Adenosine A2ATNF Receptor-Associated Factor 6arthritis, experimentalelectroacupuncturemitogen-activated protein kinasesosteoclastsreceptor, adenosine A2Asignal transduction

Identifiers

PMID37946472
PMCPMC10623259
OpenAlexW4388578679

What OpenQuestion holds

Textmetadata
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.