Pulsed Electromagnetic Field Inhibits Synovitis via Enhancing the Efferocytosis of Macrophages

Ouyang, Jingping; Zhang, Bin; Kuang, Liang; Yang, Peng; Du, Xiaolan; Qi, Huabin; Su, Nan; Jin, Min; Yang, Jing; Xie, Yangli; Tan, Qiaoyan; Chen, Hangang; Chen, Shuai; Jiang, Wanling; Liu, Mi; He, Mei; Ni, Zhenhong

doi:10.1155/2020/4307385

Cited by 12 publications

(9 citation statements)

References 66 publications

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“…In addition, several studies have documented that PEMFs can affect the phagocytic ability of macrophages 30 . Nevertheless, little is known about the function of PEMFs in microglia and their effects on hematoma clearance.…”

Section: Discussionmentioning

confidence: 99%

Pulsed Electromagnetic Fields Protect Against Brain Injury After Intracerebral Hemorrhage: Involvement Of Anti-Inflammatory Processes And Hematoma Clearance Via CD36

Yang

Wang

Liu

et al. 2021

Preprint

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Background: Intracerebral hemorrhage causes high mortality and morbidity, but its therapy methods are limited. In the present study, pulsed electromagnetic fields (PEMFs) were demonstrated to have beneficial effects on an intracerebral hemorrhage (ICH) model. This study explored the effects and underlying mechanism of PEMFs in a mouse model of ICH and cultured BV2 cells.Methods: PEMFs were applied 24 hours after collagenase-induced ICH and 4 hours per day for seven consecutive days. The levels of proinflammatory factors were assessed by ELISA kits and western blotting. Hematoma volume was measured by histological analysis. The effects of PEMFs on phagocytosis of the erythrocytes was observed in cultured BV2 cells.Results: Seven days after ICH, the hematoma volume was significantly reduced in PEMF-treated animals compared to nontreated mice. We found that PEMFs decreased the hematoma volume and the levels of proinflammatory factors after ICH. To evaluate the mechanisms underlying the effects of PEMFs on ICH, we analyzed the transcriptome profile three days after ICH, and we found that PEMFs reversed the changes in inflammation-related pathways and alleviated neurological deficits. Furthermore, PEMFs enhanced the erythrophagocytosis of microglia via CD36. Thus, the PEMF-mediated promotion of neurological functions may at least partly involve anti-inflammatory processes and hematoma clearance.Conclusions: These results suggest that PEMF treatment is a possible adjuvant therapy for ICH patients.

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Section: Discussionmentioning

confidence: 99%

Pulsed Electromagnetic Fields Protect Against Brain Injury After Intracerebral Hemorrhage: Involvement Of Anti-Inflammatory Processes And Hematoma Clearance Via CD36

Yang

Wang

Liu

et al. 2021

Preprint

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“…Additionally, the phosphorylation of p38 MAPK(ERK1/2) was shown to be inhibited by the exposure to PEMF (1.5mT; 75Hz, 10% duty cycle) in an inflammatory model of synovitis, leading to the decrease of TNF [52].…”

Section: Contributions Of Pemf Stimulation To Resolve Inflammatory Cues In Il-1β-magcssmentioning

confidence: 99%

Human tendon-derived cell sheets created by magnetic force-based tissue engineering hold tenogenic and immunomodulatory potential

et al. 2021

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“…In addition, the enhanced phagocytosis of apoptotic neutrophils by macrophages (also termed efferocytosis) has been revealed to reduce inflammation in synovitis. 103…”

Section: Peripheral Inflammation Contributes To the Pathogenesis Of C...mentioning

confidence: 99%

Inflammation in pathogenesis of chronic pain: Foe and friend

Fang,

Zhai,

Zhu

et al. 2023

Mol Pain

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Chronic pain is a refractory health disease worldwide causing an enormous economic burden on individuals and society. Accumulating evidence suggests that inflammation in the peripheral nervous system (PNS) and central nervous system (CNS) is the major factor in the pathogenesis of chronic pain. The inflammation in the early- and late phase may have distinctive effects on the initiation and resolution of pain, which can be viewed as friend or foe. On the one hand, painful injuries lead to the activation of glial cells and immune cells in the PNS, releasing pro-inflammatory mediators, which contribute to the sensitization of nociceptors, leading to chronic pain; neuroinflammation in the CNS drives central sensitization and promotes the development of chronic pain. On the other hand, macrophages and glial cells of PNS and CNS promote pain resolution via anti-inflammatory mediators and specialized pro-resolving mediators (SPMs). In this review, we provide an overview of the current understanding of inflammation in the deterioration and resolution of pain. Further, we summarize a number of novel strategies that can be used to prevent and treat chronic pain by controlling inflammation. This comprehensive view of the relationship between inflammation and chronic pain and its specific mechanism will provide novel targets for the treatment of chronic pain.

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Pulsed Electromagnetic Field Inhibits Synovitis via Enhancing the Efferocytosis of Macrophages

Cited by 12 publications

References 66 publications

Pulsed Electromagnetic Fields Protect Against Brain Injury After Intracerebral Hemorrhage: Involvement Of Anti-Inflammatory Processes And Hematoma Clearance Via CD36

Pulsed Electromagnetic Fields Protect Against Brain Injury After Intracerebral Hemorrhage: Involvement Of Anti-Inflammatory Processes And Hematoma Clearance Via CD36

Human tendon-derived cell sheets created by magnetic force-based tissue engineering hold tenogenic and immunomodulatory potential

Inflammation in pathogenesis of chronic pain: Foe and friend

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