214 THE ANALGESIC ACTION OF PULSED RADIOFREQUENCY APPLIED TO DORSAL ROOT GANGLION ON NEUROPATHIC PAIN IN RATS

2010 ◽  
Vol 4 (S1) ◽  
pp. 63-63
Author(s):  
Y.-R. Wen ◽  
M.-L. Lin ◽  
C.-W. Lin ◽  
S.-H. Huang
2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Xueru Xu ◽  
Shaoxiong Fu ◽  
Xiaomei Shi ◽  
Rongguo Liu

Background. Pulsed radiofrequency (PRF) on the dorsal root ganglion (DRG) has been applied to alleviate neuropathic pain effectively, yet the mechanisms underlying pain reduction owing to this treatment are not clarified completely. The activated microglia, brain-derived neurotrophic factor (BDNF), phosphatidylinositol 3-kinase (PI3K), and phosphorylated extracellular signal-regulated kinase (p-ERK) in the spinal cord were demonstrated to be involved in developing neuropathic pain. Also, it has been just known that PRF on DRG inhibits the microglial activation in nerve injury rats. Here, we aim to investigate whether PRF treatment could regulate the levels of BDNF, PI3K, and p-ERK in the spinal cord of rats with spared nerve injury (SNI) via suppressing the spinal microglia activation to ease neuropathic pain. Methods. The rats with SNI were intrathecally treated with minocycline (specific microglia inhibitor) or same volume of dimethyl sulfoxide once daily, beginning from 1 h before nerve transection to 7 days. PRF was applied adjacent to the L4-L5 DRG of rats with SNI at 45 V for 6 min on the seventh postoperative day, whereas the free-PRF rats were treated without PRF. The withdrawal thresholds were studied, and the spinal levels of ionized calcium-binding adapter molecule 1 (Iba1), BDNF, PI3K, and p-ERK were calculated by western blot analysis, reverse transcription-polymerase chain reaction, and immunofluorescence. Results. The paw withdrawal mechanical threshold and paw withdrawal thermal latency decreased in the ipsilateral hind paws after SNI, and the spinal levels of Iba1, BDNF, PI3K, and p-ERK increased on day 21 after SNI compared with baseline (P<0.01). An intrathecal injection of minocycline led to the reversal of SNI-induced allodynia and increase in levels of Iba1, BDNF, PI3K, and p-ERK. Withdrawal thresholds recovered partially after a single PRF treatment for 14 days, and SNI-induced microglia hyperactivity, BDNF upregulation, and PI3K and ERK phosphorylation in the spinal cord reduced on D14 due to the PRF procedure. Conclusion. Microglial BDNF, PI3K, and p-ERK in the spinal cord are suppressed by the therapy of PRF on DRG to ease SNI-induced neuropathic pain in rats.


2021 ◽  
Author(s):  
Xueru Xu ◽  
Zhisen Dai ◽  
Chun Lin ◽  
Fan Lin ◽  
Rongguo Liu

Abstract Background: Increasing evidence suggests that neuroglia, neuroimmune, and neuroinflammatory processes are involved in the development of nerve injury-induced pain and depression. Interferon regulatory factor 8 (IRF8), a crucial factor for microglial activation, is essential for the development of neuropathic pain. The brain-derived neurotrophic factor (BDNF) and inflammatory mediators (IL-1β, IL-6, and TNF-α) in the hippocampus contribute to the pathophysiology of neuropathic pain-depression comorbidity. Our previous study found that depressive-like behaviors induced by spared nerve injury (SNI) could be improved by applying pulsed radiofrequency (PRF) to the dorsal root ganglion (DRG) (PRF-DRG). However, the anti-depressive mechanisms of PRF-DRG therapy remain largely unknown. Methods: All rats (except for those in the sham group) were subjected to SNI. The nuclease-free water group and the IRF8 siRNA group were intrathecally injected with nuclease-free water and IRF8 siRNA on days 5 and 6 after SNI, respectively. PRF therapy on the L5 DRG was performed in the PRF group on day 7 after SNI, whereas no PRF current was delivered in the Sham-PRF group. The 50% paw withdrawal threshold, forced swimming test, and sucrose preference test were performed. The expression levels of spinal IRF8 and hippocampal BDNF were tested by molecular biochemistry, while IL-1β, IL-6, and TNF-α were tested by ELISA.Results: The depressive-like behaviors induced by SNI were remarkably developed in rats, which was indicated by a significant reduction in the sucrose preference rate and prolonged immobility time on day 42 after SNI. Mechanical allodynia and depression-like behaviors of rats with SNI were remarkably improved after PRF-DRG or intrathecal IRF8 siRNA. Spinal IRF8 overexpression, hippocampal BDNF downregulation, and increased hippocampal IL-1β and TNF-α levels were reversed by PRF-DRG, similar to the intrathecal injection of IRF8 siRNA. Conclusions: PRF-DRG therapy could regulate neuroimmune and neuroinflammatory responses to improve pain-induced depressive-like behaviors. The beneficial effect was correlated with the upregulation of BDNF and inhibition of IL-1β and TNF-α in the hippocampus via spinal IRF8 inactivation.


2019 ◽  
Vol 44 (7) ◽  
pp. 742-746 ◽  
Author(s):  
Ren Jiang ◽  
Ping Li ◽  
Yong-Xing Yao ◽  
Hong Li ◽  
Rongjun Liu ◽  
...  

Background and objectivesPulsed radiofrequency (PRF) is a minimal neurodestructive interventional pain therapy. However, its analgesic mechanism remains largely unclear. We aimed to investigate the peripheral and spinal mechanisms of PRF applied either adjacent to the ipsilateral L5 dorsal root ganglion (PRF-DRG) or PRF to the sciatic nerve (PRF-SN) in the neuropathic pain behavior induced by chronic constriction injury (CCI) in rats.MethodsOn day 0, CCI or sham surgeries were performed. Rats then received either PRF-DRG, PRF-SN, or sham PRF treatment on day 4. Pain behavioral tests were conducted before surgeries and on days 1, 3, 5, 7, 9, 11, 13, and 14. After the behavioral tests, the rats were sacrificed. The venous blood or sciatic nerve samples were collected for ELISAs and the dorsal horns of the L4–L6 spinal cord were collected for western blot examination.ResultsThe mechanical allodynia and the thermal hyperalgesia has been relieved by a single PRF-DRG or PRF-SN application. In addition, the analgesic effect of PRF-DRG was superior to PRF-SN on CCI-induced neuropathic pain. Either PRF-DRG or PRF-SN reversed the enhancement of interleukin 1β (IL-1β) and tumor necrosis factor alpha (TNF-α) levels in the blood of CCI rats. PRF-DRG or PRF-SN also downregulated spinal β-catenin expression.ConclusionsPRF treatment either to DRG or to sciatic nerve reduced neuropathic pain behavior, and reduced peripheral levels of pro-inflammatory cytokines and spinal β-catenin expression in CCI rats. PRF to DRG has a better analgesic effect than PRF to the nerve.


2020 ◽  
Vol 36 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Simone Vigneri ◽  
Gianfranco Sindaco ◽  
Marco La Grua ◽  
Matteo Zanella ◽  
Giuliano Lo Bianco ◽  
...  

2018 ◽  
Vol 1 (21;1) ◽  
pp. E307-E322 ◽  
Author(s):  
Ronggue Liu

Background: Interferon regulatory factor 8 (IRF8), which is induced by peripheral nerve injury (PNI), plays a key role in activating spinal microglia to release inflammatory cytokines in a p38- dependent way, thereafter results in formation of central sensitization. Pulsed radiofrequency (PRF) on dorsal root ganglion (DRG) alleviates neuropathic pain and inhibits the microglial activation in chronic constriction injury (CCI) rats. However, the consequences of PRF on spinal IRF8 of CCI rats remains unknown. Objectives: We explore if PRF on DRG of rats with CCI could restrain IRF8, microglia, and p38 hyperactivity in the spinal cord to alleviate neuropathic pain. Study Design: A randomized, controlled animal study. Setting: Department of Pain Management, Fujian Provincial Hospital, Fujian Key Laboratory of Geriatrics, Provincial Clinic College of Fujian Medical University. Methods: The changes in pain behaviors and the expressions of IRF8, Iba1 and p-p38 in the spinal cord of CCI rats which were administrated with antisense/ mismatch oligodeoxynucleotide of IRF8 were studied. Rats in CCI+AS ODN group, CCI+MM ODN group or CCI+NS group were intrathecally treated with antisense oligodeoxynucleotide of IRF8, mismatch oligodeoxynucleotide of IRF8 or same volume 0.9% NaCl once daily respectively, beginning from the day after nerve transection 12 hours and lasting for 7 days. The effects of PRF on L4-5 DRG of rats with CCI were investigated. PRF was applied adjacent to the L4-5 DRG at an intensity of 45 V for 6 minutes after CCI, whereas the control rats were treated without radiofrequency current. The withdrawal thresholds were studied and the spinal levels of IRF8, ionized calcium-binding adapter molecule 1 (Iba1, microglia characteristic marker) and p-p38 were calculated by ELISA, western blot, RT-PCR, and immunofluorescence. Results: Intrathecal administration of antisense oligodeoxynucleotide of IRF8 led to the reversal of CCI-induced allodynia, lower activation of spinal microglia and p-p38. Withdrawal thresholds were partially recovered after a single PRF treatment for 14 days. CCI-induced IRF8 upregulation, microglia hyperactivity, and p38 phosphorylation in the spinal cord were reduced due to PRF treatment. However, PRF did not alter pain behaviors and pain signals in normal rats. Limitations: In our study, one time point was selected just to assess the levels of microglia, and p-p38. The changes of IRF8, microglia, p-p38 in the ipsilateral DRG were not investigated. A more detailed study on how PRF on the DRG could further relieve NP is needed. Conclusions: Restraining IRF8, microglia and p38 hyperactivity in the spinal cord of CCI rats involved in the contribution to the long-lasting analgesia of PRF. Keywords: Neuropathic pain, pulsed radiofrequency, dorsal root ganglion,


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