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Métodos Terapêuticos e Terapias MTCI
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1.
J Tradit Chin Med ; 43(6): 1103-1109, 2023 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-37946472

RESUMO

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 p38α 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-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. RESULTS: The 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. CONCLUSIONS: EA 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.


Assuntos
Artrite Experimental , Eletroacupuntura , Proteína Quinase 14 Ativada por Mitógeno , Animais , Camundongos , Osteogênese , NF-kappa B/genética , NF-kappa B/metabolismo , Proteína Quinase 14 Ativada por Mitógeno/metabolismo , Receptor A2A de Adenosina/metabolismo , Fator 6 Associado a Receptor de TNF/genética , Diferenciação Celular , Transdução de Sinais , Ligante RANK/genética , Ligante RANK/metabolismo
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