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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

引用

Journal of Traditional Chinese Medicine 2023年第6期43卷 1103-1109页

作者： DU Zhongheng CONG Wenjie TANG Kejing ZHENG Qiqi SONG Zhiwei CHEN Yong YANG Su ZHANG Chunwu YE Tianshen Department of Acupuncture the First Affiliated Hospital of Wenzhou Medical UniversityWenzhou 325000China Department of Traditional Chinese Orthopedics&Traumatology the First Affiliated Hospital of Wenzhou Medical UniversityWenzhou 325000China Zhejiang Provincial Key Laboratory of Aging and Neurological Disorder Research the First Affiliated Hospital of Wenzhou Medical UniversityWenzhou 325000China

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 ***:Mice with collagen induced arthritis(CIA)received different *** 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)***: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 *** 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 *** were more abundant in the CIA-control and CIA-EA-SCH58261 groups than in the CIA-EA ***:EA treatment enhanced the a2aR activity and inhibited osteoclast formation by inhibition of RANKL,RANK,TRAF6,p38α,NF-κB,and ***58261 reversed the effect of *** 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

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