scholarly journals Astragalin Alleviates Neuropathic Pain by Suppressing P2X4-Mediated Signaling in the Dorsal Root Ganglia of Rats

2021 ◽  
Vol 14 ◽  
Author(s):  
Mengke Wang ◽  
Xia Cai ◽  
Yueying Wang ◽  
Shizhen Li ◽  
Na Wang ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Therapeutic Potential ◽  
Purinergic Receptor ◽  
Pain Behavior ◽  
Hek293 Cells ◽  
Protective Effects ◽  
Satellite Glial Cell ◽  
Clinical Pain

Neurologic damage often leads to neuropathic pain, for which there are no effective treatments owing to its complex pathogenesis. The purinergic receptor P2X4 is closely associated with neuropathic pain. Astragalin (AST), a compound that is used in traditional Chinese medicine, has protective effects against allergic dermatitis and neuronal injury, but its mechanism of action is not well understood. The present study investigated whether AST can alleviate neuropathic pain in a rat model established by chronic constriction injury (CCI) to the sciatic nerve. The model rats exhibited pain behavior and showed increased expression of P2X4 and the activated satellite glial cell (SGC) marker glial fibrillary acidic protein in dorsal root ganglia (DRG). AST treatment partly abrogated the upregulation of P2X4, inhibited SGC activation, and alleviated pain behavior in CCI rats; it also suppressed ATP-activated currents in HEK293 cells overexpressing P2X4. These data demonstrate that AST relieves neuropathic pain by inhibiting P2X4 and SGC activation in DRG, highlighting its therapeutic potential for clinical pain management.

scholarly journals Pentoxifylline Ameliorates Mechanical Hyperalgesia in a Rat Model of ChemotherapyInduced Neuropathic Pain

2016 ◽  
Vol 4;19 (4;5) ◽  
pp. E589-E600
Author(s):  
Salahadin Abdi
Keyword(s):  
Neuropathic Pain ◽  
Continuous Infusion ◽  
Inflammatory Cytokines ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Pain Treatment ◽  
Phosphodiesterase Inhibitor ◽  
Pain Behavior ◽  
Sprague Dawley ◽  
Tnf Α

Background: Chemotherapy-induced neuropathic pain is difficult to treat. Pentoxifylline inhibits the production of inflammatory cytokines including tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β). Objective: The aims of our study were to investigate the analgesic and preventive effects of pentoxifylline on paclitaxel-induced neuropathic pain in rats and to identify its mechanisms of action. Study Design: Controlled animal study. Methods: Neuropathic pain was induced with intraperitoneally injected paclitaxel on 4 alternate days in male Sprague-Dawley rats. Pentoxifylline was administered systemically as a single injection and a continuous infusion before or after the injection of paclitaxel. The mechanical threshold for allodynia was measured by using von Frey filaments. Protein levels and localization of inflammatory cytokines were performed by using Western blotting and immunohistochemistry, respectively. Results: After the rats developed neuropathic pain behavior, a single intraperitoneal injection and continuous infusion of pentoxifylline ameliorated paclitaxel-induced mechanical allodynia. In addition, systemic infusion of pentoxifylline in the early phase of the development of pain behavior delayed the onset of paclitaxel-induced pain behavior. Paclitaxel increased the levels of the catalytic subunit α of protein kinase A, phosphorylated nuclear factor κB, TNF-α, and IL-1β in the lumbar dorsal root ganglia. Pentoxifylline decreased the paclitaxel-induced TNF-α and IL1β levels. In addition, IL-1β was expressed in neurons and satellite cells in the lumbar dorsal root ganglia after paclitaxel. Limitations: Although this study was performed in the animal model by well-designed manner, clinical study will be needed to confirm the analgesic effect of pentoxifylline. Conclusion: Pentoxifylline alleviated chemotherapy-induced neuropathic pain in rats by reducing the levels of inflammatory cytokines in dorsal root ganglia and may be effective chemotherapyinduced neuropathic pain in patients. Key words: Chemotherapy, chronic pain, inflammatory cytokines, neuropathic pain, paclitaxel, pain behavior, pain treatment, pentoxifylline, phosphodiesterase inhibitor

lncRNA NONRATT021972 siRNA Decreases Diabetic Neuropathic Pain Mediated by the P2X3 Receptor in Dorsal Root Ganglia

2016 ◽  
Vol 54 (1) ◽  
pp. 511-523 ◽  
Author(s):  
Haiying Peng ◽  
Lifang Zou ◽  
Jinyan Xie ◽  
Hong Wu ◽  
Bing Wu ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
P2x3 Receptor ◽  
Diabetic Neuropathic Pain

scholarly journals Efficacy and safety of pulsed radiofrequency as a method of dorsal root ganglia stimulation for treatment of non-neuropathic pain: a systematic review

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Ivana Vuka ◽  
Svjetlana Došenović ◽  
Tihana Marciuš ◽  
Lejla Ferhatović Hamzić ◽  
Katarina Vučić ◽  
...  
Keyword(s):  
Systematic Review ◽  
Neuropathic Pain ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Pulsed Radiofrequency ◽  
Efficacy And Safety

scholarly journals The effect of sinomenine in diabetic neuropathic pain mediated by the P2X3 receptor in dorsal root ganglia

2017 ◽  
Vol 13 (2) ◽  
pp. 227-235 ◽  
Author(s):  
Shenqiang Rao ◽  
Shuangmei Liu ◽  
Lifang Zou ◽  
Tianyu Jia ◽  
Shanhong Zhao ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
P2x3 Receptor ◽  
Diabetic Neuropathic Pain

scholarly journals Elevated Expression of Fractalkine (CX3CL1) and Fractalkine Receptor (CX3CR1) in the Dorsal Root Ganglia and Spinal Cord in Experimental Autoimmune Encephalomyelitis: Implications in Multiple Sclerosis-Induced Neuropathic Pain

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Wenjun Zhu ◽  
Crystal Acosta ◽  
Brian MacNeil ◽  
Claudia Cortes ◽  
Howard Intrater ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Neuropathic Pain ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Protein Expression ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Autoimmune Encephalomyelitis ◽  
Receptor Cx3cr1 ◽  
Experimental Autoimmune

Multiple sclerosis (MS) is a central nervous system (CNS) disease resulting from a targeted autoimmune-mediated attack on myelin proteins in the CNS. The release of Th1 inflammatory mediators in the CNS activates macrophages, antibodies, and microglia resulting in myelin damage and the induction of neuropathic pain (NPP). Molecular signaling through fractalkine (CX3CL1), a nociceptive chemokine, via its receptor (CX3CR1) is thought to be associated with MS-induced NPP. An experimental autoimmune encephalomyelitis (EAE) model of MS was utilized to assess time dependent gene and protein expression changes of CX3CL1 and CX3CR1. Results revealed significant increases in mRNA and the protein expression of CX3CL1 and CX3CR1 in the dorsal root ganglia (DRG) and spinal cord (SC) 12 days after EAE induction compared to controls. This increased expression correlated with behavioural thermal sensory abnormalities consistent with NPP. Furthermore, this increased expression correlated with the peak neurological disability caused by EAE induction. This is the first study to identify CX3CL1 signaling through CX3CR1 via the DRG /SC anatomical connection that represents a critical pathway involved in NPP induction in an EAE model of MS.

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