ArticleEuropean journal of medical research2024
Pulsed radiofrequency alleviates neuropathic pain by upregulating MG53 to inhibit microglial activation.
Article in European journal of medical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Pulsed Radiofrequency for Post-Stroke Complications: From Neuromodulation to Functional Recovery.Current neurology and neuroscience reports · 2026Review
- MG53, a Regenerative Myokine Linking Skeletal Muscle to Cardiac Repair.Biomolecules · 2026Review
- Targeting endoplasmic reticulum stress: a novel therapeutic strategy for neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2026Review
- Peripheral neuromodulation in spasticity-plus syndrome: effects of pulsed radiofrequency on tonic-painful disorders in multiple sclerosis.Frontiers in neurology · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
backgroundPatients with neuropathic pain (NP) have significantly lower quality of life. Because the pathophysiology of NP is not fully understood, there is a lack of effective treatment for it in clinic. This study set out to investigate the precise mechanism by which pulsed radiofrequency (PRF) alleviated NP.
methodThe rat models of chronic constriction injury of the sciatic nerve (CCI) were established to simulate the occurrence of NP, following with measuring MWT and TWL to evaluate the pain of the rats. HE staining was utilized to observe the rat spinal cord tissue pathology. The expression of MG53, ATF4 and CHOP was evaluated by qRT-PCR and WB, while the expression of inflammatory factors was measured by ELISA. In addition, immunofluorescence assay was used to detect the expression of MG53 and Iba-1.
resultPRF treatment alleviated NP in CCI rats, as well as upregulating the expression of MG53 and inhibiting microglial activation. After MG53 knockdown, the remission of NP by PRF was significantly weakened, but microglial activation and endoplasmic reticulum stress (ERS) exhibited enhancement. Therefore, PRF inhibited microglial activation by upregulating MG53. After injection of ERS inducer in CCI rats, the inhibition effect of overexpressed MG53 on microglial activation and its alleviation effect on NP were reversed. Consequently, MG53 played a role in suppressing microglial activation by mediating the inhibition of ERS.
conclusionPRF attenuated microglial activation by upregulating MG53 to inhibit ERS, resulting in the alleviation of NP in CCI rats.
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