Pulsed Electromagnetic Field Inhibits Synovitis via Enhancing the Efferocytosis of Macrophages
Pulsed Electromagnetic Field Inhibits Synovitis via Enhancing the Efferocytosis of Macrophages
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脉冲电磁场通过增强巨噬细胞的胞吞作用抑制滑膜炎
DOI：
10.1155/2020/4307385
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发表时间：
2020
影响因子：
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通讯作者：
Lin Chen
中科院分区：
文献类型：
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作者：
Junjie Ouyang;Bin Zhang;Liang Kuang;Peng Yang;Xiaolan Du;Huabin Qi;Nan Su;Min Jin;Jing Yang;Yangli Xie;Lin Chen;Hangang Chen;Shuai Chen;Wanling Jiang;Mi Liu;Xiaoqing Luo;Mei He;Zhenhong Ni;Lin Chen
滑膜炎在关节炎的发病机制中占有重要地位，与患者的关节肿胀和疼痛密切相关。本研究旨在探讨脉冲电磁场（PEMF）对滑膜炎的抗炎作用及其机制。建立内侧半月板不稳定（DMM）模型和气囊炎症模型，诱导C57 BL/6小鼠滑膜炎。然后通过PEMF（脉冲波形，1.5mT，75 Hz，10%占空比）处理小鼠。滑膜炎评分以及IL-1β和TNF-α水平表明PEMF减轻了滑膜炎的严重程度。此外，中性粒细胞在滑膜样层的比例减少，而巨噬细胞的比例增加后，PEMF治疗。此外，PEMF增强了巨噬细胞对凋亡中性粒细胞的吞噬作用。Western blot结果显示，PEMF可抑制P38的磷酸化。总之，我们目前的数据表明，PEMF非侵入性地通过上调巨噬细胞中的巨噬细胞增多而对滑膜炎表现出抗炎作用，这可能涉及P38的磷酸化。
Synovitis plays an important role in the pathogenesis of arthritis, which is closely related to the joint swell and pain of patients. The purpose of this study was to investigate the anti-inflammatory effects of pulsed electromagnetic fields (PEMF) on synovitis and its underlying mechanisms. Destabilization of the medial meniscus (DMM) model and air pouch inflammation model were established to induce synovitis in C57BL/6 mice. The mice were then treated by PEMF (pulse waveform, 1.5 mT, 75 Hz, 10% duty cycle). The synovitis scores as well as the levels of IL-1β and TNF-α suggested that PEMF reduced the severity of synovitis in vivo. Moreover, the proportion of neutrophils in the synovial-like layer was decreased, while the proportion of macrophages increased after PEMF treatment. In addition, the phagocytosis of apoptotic neutrophils by macrophages (efferocytosis) was enhanced by PEMF. Furthermore, the data from western blot assay showed that the phosphorylation of P38 was inhibited by PEMF. In conclusion, our current data show that PEMF noninvasively exhibits the anti-inflammatory effect on synovitis via upregulation of the efferocytosis in macrophages, which may be involved in the phosphorylation of P38.