观察电针（EA）刺激足三里（ST36）、三阴交（SP6）对破骨细胞生成的抑制作用以及腺苷A2A受体（A2AR）和p38α丝裂原激活蛋白激酶（MAPK）信号通路在介导此过程中的作用。效果。患有胶原诱导关节炎（CIA）的小鼠接受了不同的治疗。采用免疫组织化学和蛋白质印迹法测定这些关节中多种信号分子的水平[核转录因子-κB受体激活剂（NF-κB）配体（RANKL）、NF-κB受体激活剂（RANK）、肿瘤坏死因子受体相关因子 6 (TRAF6)、p38α、NF-κB 和活化 T 细胞核因子 C1 (NFATc1)]。使用抗酒石酸酸性磷酸酶 (TRAP) 染色鉴定破骨细胞。免疫组织化学结果表明 CIA 对照组和 CIA-EA-SCH58261 组中 p38α、NF-κB 和 NFATc1 上调，但 CIA-EA 组中水平降低。蛋白质印迹表明 CIA 对照组和 CIA-EA-SCH58261 组中 RANKL、RANK、TRAF6、p38α、NF-κB 和 NFATc1 表达上调，但 CIA-EA 组中表达降低。 CIA 对照组和 CIA-EA-SCH58261 组的破骨细胞比 CIA-EA 组更丰富。 EA 治疗增强了 A2AR 活性，并通过抑制 RANKL、RANK、TRAF6、p38α、NF-κB 和NFATc1。 SCH58261逆转了EA的效果。这些结果表明 EA 通过增加 A2AR 活性来调节 p38α-MAPK 信号传导，从而抑制破骨细胞生成。

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.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.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.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.