Electroacupuncture stimulating Zusanli(ST36),Sanyinjiao(SP6)in mice with collagen-induced arthritis leads to adenosine A2A receptor-mediated alteration of p38αmitogen-activated protein kinase signaling and inhibition of osteoclastogenesis  

作　　者：DU Zhongheng CONG Wenjie TANG Kejing ZHENG Qiqi SONG Zhiwei CHEN Yong YANG Su ZHANG Chunwu YE Tianshen 

机构地区：[1]Department of Acupuncture,the First Affiliated Hospital of Wenzhou Medical University,Wenzhou 325000,China [2]Department of Traditional Chinese Orthopedics&Traumatology,the First Affiliated Hospital of Wenzhou Medical University,Wenzhou 325000,China [3]Zhejiang Provincial Key Laboratory of Aging and Neurological Disorder Research,the First Affiliated Hospital of Wenzhou Medical University,Wenzhou 325000,China

出　　处：《Journal of Traditional Chinese Medicine》2023年第6期1103-1109,共7页中医杂志（英文版）

基　　金：National Natural Science Foundation of China:the Mechanism of Adenosine A2A Receptor Modulate Electroacupuncture Inhibiting Osteoclast Formation in Mice with Collagen-Induced Arthritis (No.81674053);Zhejiang Basic Public Welfare Research Project:the Role of P38 MAPK Pathway in the Inhibition of CIA Osteoclast Differentiation by Electroacupuncture via Adenosine Pathway (No.LY20H270015);Basic Medical and Health Technology Project of Wenzhou Science and Technology Bureau:Electroacupuncture of Mice with CIA Mitigate Joint Damage by the p38MAPK Pathway (No.Y20190198);Scientific Research Incubation Project of the First Affiliated Hospital of Wenzhou Medical University:Electroacupuncture of Mice with CIA Mitigate Joint Damage by the p38MAPK Pathway (No.FHY2019021)

摘　　要：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 p38αMitogen-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.

关 键 词：ELECTROACUPUNCTURE arthritis experimental receptor adenosine A2A mitogen-activated protein kinases signal transduction OSTEOCLASTS 

分 类 号：R245[医药卫生—针灸推拿学]