PMID- 37946472
OWN - NLM
STAT- MEDLINE
DCOM- 20231113
LR  - 20231113
IS  - 2589-451X (Electronic)
IS  - 0255-2922 (Print)
IS  - 0255-2922 (Linking)
VI  - 43
IP  - 6
DP  - 2023 Oct
TI  - Electroacupuncture stimulating Zusanli (ST36), Sanyinjiao (SP6) in mice with 
      collagen-induced arthritis leads to adenosine A2A receptor-mediated alteration of 
      p38alpha mitogen-activated protein kinase signaling and inhibition of 
      osteoclastogenesis.
PG  - 1103-1109
LID - 10.19852/j.cnki.jtcm.2023.06.001 [doi]
AB  - OBJECTIVE: To 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 p38alpha Mitogen-Activated Protein Kinase 
      (MAPK) signaling pathway in mediating this effect. METHODS: Mice 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-kappaB 
      (NF-kappaB) ligand (RANKL), receptor activator of NF-kappaB (RANK), tumor necrosis factor 
      receptor associated factor 6 (TRAF6), p38alpha, NF-kappaB, and nuclear factor of 
      activated T cells C1 (NFATc1)]. Osteoclasts were identified using 
      tartrate-resistant acid phosphatase (TRAP) staining. RESULTS: The 
      immunohistochemistry results indicated upregulation of p38alpha, NF-kappaB, 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, p38alpha, 
      NF-kappaB, 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. CONCLUSIONS: EA treatment 
      enhanced the A2AR activity and inhibited osteoclast formation by inhibition of 
      RANKL, RANK, TRAF6, p38alpha, NF-kappaB, and NFATc1. SCH58261 reversed the effect of EA. 
      These results suggest that EA regulated p38alpha-MAPK signaling by increasing A2AR 
      activity, which inhibited osteoclastogenesis.
FAU - Zhongheng, D U
AU  - Zhongheng DU
AD  - Department of Acupuncture, the First Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou 325000, China.
FAU - Wenjie, Cong
AU  - Wenjie C
AD  - Department of Acupuncture, the First Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou 325000, China.
FAU - Kejing, Tang
AU  - Kejing T
AD  - Department of Acupuncture, the First Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou 325000, China.
FAU - Qiqi, Zheng
AU  - Qiqi Z
AD  - Department of Acupuncture, the First Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou 325000, China.
FAU - Zhiwei, Song
AU  - Zhiwei S
AD  - Department of Acupuncture, the First Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou 325000, China.
FAU - Yong, Chen
AU  - Yong C
AD  - Department of Acupuncture, the First Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou 325000, China.
FAU - Su, Yang
AU  - Su Y
AD  - Zhejiang Provincial Key Laboratory of Aging and Neurological Disorder Research, 
      the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, 
      China.
FAU - Chunwu, Zhang
AU  - Chunwu Z
AD  - Department of Traditional Chinese Orthopedics & Traumatology, the First 
      Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
FAU - Tianshen, Y E
AU  - Tianshen YE
AD  - Department of Acupuncture, the First Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou 325000, China.
LA  - eng
GR  - 81674053/Mechanism of Adenosine A2A Receptor Modulate Electroacupuncture 
      Inhibiting Osteoclast Formation in Mice with Collagen-Induced Arthritis/
GR  - LY20H270015/Role of P38 MAPK Pathway in the Inhibition of CIA Osteoclast 
      Differentiation by Electroacupuncture via Adenosine Pathway/
GR  - Y20190198/Electroacupuncture of Mice with CIA Mitigate Joint Damage by the 
      p38MAPK Pathway/
GR  - FHY2019021/Electroacupuncture of Mice with CIA Mitigate Joint Damage by the 
      p38MAPK Pathway/
PT  - Journal Article
PL  - China
TA  - J Tradit Chin Med
JT  - Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan
JID - 8211546
RN  - 0 (NF-kappa B)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 14)
RN  - 0 (Receptor, Adenosine A2A)
RN  - 0 (TNF Receptor-Associated Factor 6)
RN  - 0 (RANK Ligand)
SB  - IM
MH  - Animals
MH  - Mice
MH  - Osteogenesis
MH  - NF-kappa B/genetics/metabolism
MH  - *Arthritis, Experimental
MH  - *Mitogen-Activated Protein Kinase 14/metabolism
MH  - Receptor, Adenosine A2A/metabolism
MH  - TNF Receptor-Associated Factor 6/genetics
MH  - *Electroacupuncture
MH  - Cell Differentiation
MH  - Signal Transduction
MH  - RANK Ligand/genetics/metabolism
PMC - PMC10623259
OTO - NOTNLM
OT  - arthritis, experimental
OT  - electroacupuncture
OT  - mitogen-activated protein kinases
OT  - osteoclasts
OT  - receptor, adenosine A2A
OT  - signal transduction
EDAT- 2023/11/10 06:44
MHDA- 2023/11/13 06:42
PMCR- 2023/10/25
CRDT- 2023/11/10 03:39
PHST- 2023/11/13 06:42 [medline]
PHST- 2023/11/10 06:44 [pubmed]
PHST- 2023/11/10 03:39 [entrez]
PHST- 2023/10/25 00:00 [pmc-release]
AID - 1698986587282-151386573 [pii]
AID - JTCM-43-6-1103 [pii]
AID - 10.19852/j.cnki.jtcm.2023.06.001 [doi]
PST - ppublish
SO  - J Tradit Chin Med. 2023 Oct;43(6):1103-1109. doi: 
      10.19852/j.cnki.jtcm.2023.06.001.