scholarly journals Preliminary Study on Pain Reduction of Monosodium Iodoacetate-Induced Knee Osteoarthritis in Rats by Carbon Dioxide Laser Moxibustion

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Fan Wu ◽  
Ruixing Zhang ◽  
Xueyong Shen ◽  
Lixing Lao
Keyword(s):  
Treatment Group ◽  
Knee Osteoarthritis ◽  
Dorsal Horn ◽  
Carbon Dioxide Laser ◽  
Spinal Dorsal Horn ◽  
Pain Reduction ◽  
Control Group ◽  
Blank Control Group ◽  
Spinal Dorsal ◽  
Monosodium Iodoacetate

In order to study the effects of CO2laser moxibustion on the pain and inflammatory cytokine expression in the spinal dorsal horn of rats with monosodium iodoacetate- (MIA-) induced knee osteoarthritis (KOA), we designed an experiment by randomly assigning 8 SD rats into 3 groups, namely, a CO2laser moxibustion group, a sham treatment group, and a blank control group. The treatment group received a laser moxibustion on acupoint Dubi (ST 35; 5 min/treatment, 1 treatment/day) for 8 days, and after treatment, the rats exhibited significantly increased interhindpaw differences compared with their preinduction values. Meanwhile, cytokine microarray analysis showed that one cytokine (TIMP-1) was significantly upregulated and two cytokines (Agrin and MMP-8) were significantly downregulated in treatment group. The present study suggested that CO2laser moxibustion created certain pain reduction in the rats with MIA-induced KOA and significantly inhibited the expression of most inflammatory cytokines in the ipsilateral spinal dorsal horn.

Effects of Halothane and Isoflurane on Hyperexcitability of Spinal Dorsal Horn Neurons after Incision in the Rat

2005 ◽  
Vol 102 (1) ◽  
pp. 165-174 ◽  
Author(s):  
Mikito Kawamata ◽  
Eichi Narimatsu ◽  
Yuji Kozuka ◽  
Toshiyuki Takahashi ◽  
Shigekazu Sugino ◽  
...  
Keyword(s):  
Spontaneous Activity ◽  
Dorsal Horn ◽  
Neuronal Activity ◽  
Spinal Dorsal Horn ◽  
Dynamic Range ◽  
Field Size ◽  
Control Group ◽  
Sprague Dawley ◽  
Dorsal Horn Neurons ◽  
Spinal Dorsal

Background The aim of this study was to determine whether halothane and isoflurane used during and after surgical injury attenuate subsequent hyperexcitability of spinal dorsal horn (SDH) neurons by preventing development of central sensitization. Methods Activity of a wide-dynamic-range neuron of the SDH was isolated in decerebrate-spinal Sprague-Dawley rats, and neuronal activity (receptive field size and responses to nonnoxious and noxious stimuli) was recorded. A 1-cm-long incision was made through the skin, fascia, and muscle under anesthesia with halothane (1.1% or 2.2%) and isoflurane (1.4% or 2.8%). Anesthesia was discontinued just after the incision had been made or was continued until 30 min after the incision, and activity of the SDH neurons was measured for up to 2 h after the incision. In a control group, the incision was made without anesthesia. Results In the control group, the incision resulted in maximum excitation in the SDH neurons during surgery; spontaneous activity significantly increased for up to 30 min after the incision (P < 0.05) but did not significantly increase thereafter, returning to the preincision value. Halothane and isoflurane suppressed excitation of the neurons during the incision in a concentration-related manner. Administration of 2.2% halothane and 2.8% isoflurane during the incision and for up to 30 min after the incision almost abolished activity of the neurons for 30 min after the incision. The magnitude of neuronal activity 2 h after the incision was not significantly different among all groups, including the control group. Conclusions The results demonstrate that administration of halothane and isoflurane does not attenuate development of hyperexcitability of SDH neurons despite the fact that excitation and spontaneous activity during and after the incision were greatly suppressed by administration of halothane and isoflurane.

scholarly journals Role of Primary Afferents in Arthritis Induced Spinal Microglial Reactivity

2021 ◽  
Vol 12 ◽  
Author(s):  
Charlie H. T. Kwok ◽  
Yuta Kohro ◽  
Michael Mousseau ◽  
Melissa S. O’Brien ◽  
John R. Matyas ◽  
...  
Keyword(s):  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Atp Release ◽  
Afferent Input ◽  
Female Rats ◽  
Male Rats ◽  
Joint Injury ◽  
Joint Afferents ◽  
Spinal Dorsal ◽  
Monosodium Iodoacetate

Increased afferent input resulting from painful injury augments the activity of central nociceptive circuits via both neuron-neuron and neuron-glia interactions. Microglia, resident immune cells of the central nervous system (CNS), play a crucial role in the pathogenesis of chronic pain. This study provides a framework for understanding how peripheral joint injury signals the CNS to engage spinal microglial responses. During the first week of monosodium iodoacetate (MIA)-induced knee joint injury in male rats, inflammatory and neuropathic pain were characterized by increased firing of peripheral joint afferents. This increased peripheral afferent activity was accompanied by increased Iba1 immunoreactivity within the spinal dorsal horn indicating microglial activation. Pharmacological silencing of C and A afferents with co-injections of QX-314 and bupivacaine, capsaicin, or flagellin prevented the development of mechanical allodynia and spinal microglial activity after MIA injection. Elevated levels of ATP in the cerebrospinal fluid (CSF) and increased expression of the ATP transporter vesicular nucleotide transporter (VNUT) in the ipsilateral spinal dorsal horn were also observed after MIA injections. Selective silencing of primary joint afferents subsequently inhibited ATP release into the CSF. Furthermore, increased spinal microglial reactivity, and alleviation of MIA-induced arthralgia with co-administration of QX-314 with bupivacaine were recapitulated in female rats. Our results demonstrate that early peripheral joint injury activates joint nociceptors, which triggers a central spinal microglial response. Elevation of ATP in the CSF, and spinal expression of VNUT suggest ATP signaling may modulate communication between sensory neurons and spinal microglia at 2 weeks of joint degeneration.

scholarly journals Analgesic Effect of Boiogito, a Japanese Traditional Kampo Medicine, on Post-Traumatic Knee Osteoarthritis through Inhibition of ERK1/2 Phosphorylation in the Dorsal Horn of the Spinal Cord

2021 ◽  
Vol 11 (18) ◽  
pp. 8421
Author(s):  
Yusuke Kunieda ◽  
Takayuki Okumo ◽  
Hideshi Ikemoto ◽  
Naoki Adachi ◽  
Midori Tanaka ◽  
...  
Keyword(s):  
Knee Osteoarthritis ◽  
Dorsal Horn ◽  
Western Blotting ◽  
Spinal Dorsal Horn ◽  
Kinase Inhibitor ◽  
Mitogen Activated Protein Kinase ◽  
Rotarod Test ◽  
Spinal Dorsal ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

Boiogito (BO), a Japanese traditional herbal medicine, has been proven to be clinically effective against knee osteoarthritis (KOA)-associated pain. However, the therapeutic mechanism of BO remains unclear. Thus, we investigated the analgesic mechanism of BO using a rat KOA model. KOA was induced by destabilization of the medial meniscus (DMM). Rats were allocated into the following four groups: control, sham, DMM, and DMM + BO groups. Rotarod test was performed to evaluate the pain-related locomotive dysfunction. Expression of phosphorylated extracellular signal-regulated kinase1/2 (pERK1/2) in the spinal dorsal horn was examined using immunofluorescence staining and Western blotting on days 1 and 28 after DMM surgery. A mitogen-activated protein kinase inhibitor, U0126, was intrathecally injected and rotarod test and Western blotting were performed. The rotarod test revealed hampered locomotive function in the DMM group, which was significantly improved upon BO administration. The number of pERK1/2-positive cells was increased in the DMM group, whereas it was significantly decreased in the DMM + BO group. U0126 significantly inhibited ERK1/2 phosphorylation and increased walking time in the rotarod test, suggesting that the DMM-related pain was associated with ERK1/2 phosphorylation in the spinal dorsal horn. In conclusion, BO administration improved the pain-related locomotive dysfunction by suppressing ERK1/2 phosphorylation.

scholarly journals Blockade of Erythropoietin-Producing Human Hepatocellular Carcinoma Receptor B1 in Spinal Dorsal Horn Alleviates Visceral Pain in Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Chen-Li Sun ◽  
Cheng-Wen Li ◽  
Nong He ◽  
Yuan-Zhang Tang ◽  
Xiu-Liang Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Visceral Pain ◽  
Intrathecal Administration ◽  
Human Hepatocellular Carcinoma ◽  
Control Group ◽  
Visceral Hyperalgesia ◽  
Spinal Dorsal ◽  
Phosphorylated Form

Objective. This experiment was designed to determine whether erythropoietin-producing human hepatocellular carcinoma (Eph) receptors were involved in the development of visceral pain. Methods. Adult male Sprague-Dawley rats were randomly divided into three groups receiving different treatments (n = 16 per group): intracolonic vehicle (control group), intracolonic 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) (TNBS group), and intracolonic TNBS and intrathecal EphB1 receptor blocking reagent (TNBS + EphB2-Fc group). Visceral hyperalgesia was evaluated with quantification of visceral pain threshold induced by colorectal distention. The spinal expressions of EphB1 and ephrinB2 and levels of their phosphorylated forms (p-EphB1 and p-ephrinB2) were assessed by Western blotting and immunohistochemistry. Results. The TNBS-treated rats developed significant visceral hyperalgesia. The spinal expressions of EphB1, p-EphB1, ephrinB2, and p-ephrinB2 were significantly increased in the TNBS group compared with the control group, but visceral hyperalgesia and elevation of spinal EphB1 and p-EphB1 expressions were evidently alleviated by intrathecal administration of EphB2-Fc in the TNBS + EphB2-Fc group. The number of EphB1- and p-EphB1-immunopositive cells, the average optical (AO) value of EphB1, and its phosphorylated form in the spinal dorsal horn were significantly increased in the TNBS group than in the control group, but they were obviously reduced by intrathecal administration of EphB2-Fc. There were no significant differences in the number of ephrinB2- and p-ephrinB2-immunopositive cells and the AO value of ephrinB2 and its phosphorylated form between the TNBS and TNBS + EphB2-Fc groups. Conclusion. EphB1 receptors in the spinal dorsal horn play a pivotal role in the development of visceral pain and may be considered as a potential target for the treatment of visceral pain.

scholarly journals Calcitonin gene-related peptide regulates spinal microglial activation through the histone H3 lysine 27 trimethylation via enhancer of zeste homolog-2 in rats with neuropathic pain

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Qi An ◽  
Chenyan Sun ◽  
Ruidi Li ◽  
Shuhui Chen ◽  
Xinpei Gu ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Horn ◽  
Nerve Injury ◽  
Spinal Dorsal Horn ◽  
Microglial Activation ◽  
Microglial Cells ◽  
Gene Promoters ◽  
Spinal Dorsal ◽  
Related Peptide ◽  
Calcitonin Gene

Abstract Background Calcitonin gene-related peptide (CGRP) as a mediator of microglial activation at the transcriptional level may facilitate nociceptive signaling. Trimethylation of H3 lysine 27 (H3K27me3) by enhancer of zeste homolog 2 (EZH2) is an epigenetic mark that regulates inflammatory-related gene expression after peripheral nerve injury. In this study, we explored the relationship between CGRP and H3K27me3 in microglial activation after nerve injury, and elucidated the underlying mechanisms in the pathogenesis of chronic neuropathic pain. Methods Microglial cells (BV2) were treated with CGRP and differentially enrichments of H3K27me3 on gene promoters were examined using ChIP-seq. A chronic constriction injury (CCI) rat model was used to evaluate the role of CGRP on microglial activation and EZH2/H3K27me3 signaling in CCI-induced neuropathic pain. Results Overexpressions of EZH2 and H3K27me3 were confirmed in spinal microglia of CCI rats by immunofluorescence. CGRP treatment induced the increased of H3K27me3 expression in the spinal dorsal horn and cultured microglial cells (BV2) through EZH2. ChIP-seq data indicated that CGRP significantly altered H3K27me3 enrichments on gene promoters in microglia following CGRP treatment, including 173 gaining H3K27me3 and 75 losing this mark, which mostly enriched in regulation of cell growth, phagosome, and inflammation. qRT-PCR verified expressions of representative candidate genes (TRAF3IP2, BCL2L11, ITGAM, DAB2, NLRP12, WNT3, ADAM10) and real-time cell analysis (RTCA) verified microglial proliferation. Additionally, CGRP treatment and CCI increased expressions of ITGAM, ADAM10, MCP-1, and CX3CR1, key mediators of microglial activation in spinal dorsal horn and cultured microglial cells. Such increased effects induced by CCI were suppressed by CGRP antagonist and EZH2 inhibitor, which were concurrently associated with the attenuated mechanical and thermal hyperalgesia in CCI rats. Conclusion Our findings highly indicate that CGRP is implicated in the genesis of neuropathic pain through regulating microglial activation via EZH2-mediated H3K27me3 in the spinal dorsal horn.

Driving effect of BDNF in the spinal dorsal horn on neuropathic pain

2021 ◽  
pp. 135965
Author(s):  
Zhou Wu ◽  
Xie Zhiping ◽  
Li Chengcai ◽  
Zelong Xing ◽  
Xie Shenke ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Spinal Dorsal
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