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Condition: Back Pain

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Total 191 results found since Jan 2013.

The time-course and RNA interference of TNF-α, IL-6, and IL-1β expression on neuropathic pain induced by L5 spinal nerve transection in rats.
CONCLUSIONS: The time courses of TNF-α, IL-6 and IL-1β mRNA expression after L5 SNT differ. RNA interference may be a method of reducing the development of mechanical allodynia and hyperalgesia in response to nerve injury. PMID: 25844135 [PubMed]
Source: Korean Journal of Anesthesiology - November 18, 2015 Category: Anesthesiology Tags: Korean J Anesthesiol Source Type: research

Downregulation of the spinal dorsal horn clock gene Per1 expression leads to mechanical hypersensitivity via c-jun N-terminal kinase and CCL2 production in mice
Publication date: Available online 23 January 2016 Source:Molecular and Cellular Neuroscience Author(s): Norimitsu Morioka, Munenori Saeki, Tatsuhiko Sugimoto, Takuya Higuchi, Fang Fang Zhang, Yoki Nakamura, Kazue Hisaoka-Nakashima, Yoshihiro Nakata Disturbances of circadian rhythm and dysregulation of clock gene expression are involved in the induction of various neurological disorder states, including chronic pain. However, the relationship between the CNS circadian-clock gene system and nociception remains poorly defined. Significant circadian oscillations of Period (Per1, Per2), Bmal1 and Cryptochrome 1 (Cry1...
Source: Molecular and Cellular Neuroscience - January 25, 2016 Category: Neuroscience Source Type: research

Positive feedback regulation between microRNA‐132 and CREB in spinal cord contributes to bone cancer pain in mice
ConclusionsThese findings suggest that activation of spinal CREB/CRTC1 signalling may play an important role in bone cancer pain. Interruption to the positive feedback regulation between CREB/CRTC1 and its target gene miR‐132 can effectively relieved the bone cancer‐induced mechanical allodynia and spontaneous pain. What does this study add?The positive feedback regulation between CREB/CRTC1 and its target gene miR‐132 in spinal cord plays an important role in bone cancer pain.
Source: European Journal of Pain - February 26, 2016 Category: Anesthesiology Authors: B. Hou, X. Cui, Y. Liu, W. Zhang, M. Liu, Y.E. Sun, Z. Ma, X. Gu Tags: Original Article Source Type: research

CREB-regulated transcription coactivator 1 enhances CREB-dependent gene expression in spinal cord to maintain the bone cancer pain in mice
Conclusions Upregulation of CRTC1 enhancing CREB-dependent gene transcription in spinal cord may play an important role in bone cancer pain. Inhibition of spinal CRTC1 expression reduced bone cancer pain. Interruption to the positive feedback circuit between CREB/CRTC1 and its targets may contribute to the analgesic effects. These findings may provide further insight into the mechanisms and treatment of bone cancer pain.
Source: Molecular Pain - April 7, 2016 Category: Molecular Biology Authors: Liang, Y., Liu, Y., Hou, B., Zhang, W., Liu, M., Sun, Y.-E., Ma, Z., Gu, X. Tags: Research Article Source Type: research

Positive feedback regulation between microRNA ‐132 and CREB in spinal cord contributes to bone cancer pain in mice
ConclusionsThese findings suggest that activation of spinal CREB/CRTC1 signalling may play an important role in bone cancer pain. Interruption to the positive feedback regulation between CREB/CRTC1 and its target gene miR‐132 can effectively relieved the bone cancer‐induced mechanical allodynia and spontaneous pain. What does this study add?The positive feedback regulation between CREB/CRTC1 and its target gene miR‐132 in spinal cord plays an important role in bone cancer pain.
Source: European Journal of Pain - February 25, 2016 Category: Anesthesiology Authors: B. Hou, X. Cui, Y. Liu, W. Zhang, M. Liu, Y.E. Sun, Z. Ma, X. Gu Tags: Original Article Source Type: research

Annexin A10 is involved in the development and maintenance of neuropathic pain in mice
We examined the gene expressions of the L5 spinal cord after spinal nerve ligation (SNL)-induced neuropathic pain in mice by gene chip. The results showed that Anxa10 mRNA was the most upregulated gene in annexin family with 73.7-fold increase. Although previous studies have reported that several annexins are involved in nociceptive pain, the role of Anxa10 in pain remains undefined. We aimed to evaluate the role of ANXA10 in mediating injury-induced heat hyperalgesia and mechanical allodynia. We found that SNL induced persistent upregulation of Anxa10 mRNA and protein in the spinal cord of mice. Moreover, ANXA10 was coloc...
Source: Neuroscience Letters - August 9, 2016 Category: Neuroscience Source Type: research

Epigenetic suppression of potassium ‐chloride co‐transporter 2 expression in inflammatory pain induced by complete Freund's adjuvant (CFA)
ConclusionThese findings suggest that the transcription of spinal KCC2 is regulated by histone acetylation epigenetically following CFA. SignificancePersistent pain suppresses KCC2 expression through HDAC‐mediated histone hypoacetylation and consequently impairs the inhibitory function of inhibitory interneurons. Drugs such as HDAC inhibitors that suppress the influences of persistent pain on the expression of KCC2 may serve as a novel analgesic.
Source: European Journal of Pain - August 10, 2016 Category: Anesthesiology Authors: C. ‐R. Lin, J.‐K. Cheng, C.‐H. Wu, K.‐H. Chen, C.‐K. Liu Tags: Original Article Source Type: research

Cutaneous inflammation regulates THIK1 expression in small C-like nociceptor dorsal root ganglion neurons
In this study we aimed to identify the currently unknown DRG subpopulations expressing THIK1, and to investigate the relationship between the channel and both inflammatory and spontaneous pain in normal rats. Using a combination of immunohistochemistry, western blotting and behavioural tests, we found that all small neurons and large groups of medium and large DRG neurons express THIK1. Myelinated and unmyelinated fibers, nerve endings in the skin and lamina I and II of the spinal cord also express the channel. THIK1 staining co-localizes with IB4-binding and trkA suggesting that the channel is expressed by nociceptors. At...
Source: Molecular and Cellular Neuroscience - July 2, 2017 Category: Neuroscience Source Type: research

Downregulation of spinal astrocytic connexin43 leads to upregulation of interleukin ‐6 and cyclooxygenase‐2 and mechanical hypersensitivity in mice
Abstract Connexin43 (Cx43), involved in intercellular signaling, is expressed in spinal dorsal horn astrocytes and crucial in the maintenance of neuropathic pain. Downregulation of spinal astrocytic Cx43 in mice enhances glutamatergic neurotransmission by decreasing glutamate transporter GLT‐1 expression, resulting in cutaneous hypersensitivity. Decreased expression of astrocytic Cx43 could lead to altered expression of other nociceptive molecules. Transfection of Cx43‐targeting siRNA in cultured spinal astrocytes increased expression of the pronociceptive cytokine interleukin‐6 (IL‐6) and the prostaglandin synthes...
Source: Glia - November 6, 2017 Category: Neurology Authors: Norimitsu Morioka, Shiori Fujii, Syun Kondo, Fang Fang Zhang, Kazuki Miyauchi, Yoki Nakamura, Kazue Hisaoka ‐Nakashima, Yoshihiro Nakata Tags: RESEARCH ARTICLE Source Type: research

Increased Neuroligin 2 Levels in the Postsynaptic Membrane in Spinal Dorsal Horn may Contribute to Postoperative Pain
Publication date: 1 July 2018 Source:Neuroscience, Volume 382 Author(s): Ruijuan Guo, Huili Li, Xueyang Li, Yuqing Sun, Huihui Miao, Danxu Ma, Fangxiao Hong, Ye Zhang, Yun Guan, Junfa Li, Ming Tian, Yun Wang Neuroligin 2 is a synaptic cell adhesion molecule that is mainly located in inhibitory synapses and is crucial in the regulation of synapse function through protein–protein interactions. However, researchers have not clearly determined whether neuroligin 2 is involved in the development of postoperative pain. In the current study, Western blot, immunofluorescence staining and co-immunoprecipitation were used to exam...
Source: Neuroscience - May 7, 2018 Category: Neuroscience Source Type: research

Translocation Associated Membrane Protein 1 Contributes to Chronic Constriction Injury-Induced Neuropathic Pain in the Dorsal Root Ganglion and Spinal Cord in Rats
AbstractNeuropathic pain is a severe debilitating state caused by injury or dysfunction of somatosensory nervous system, and the clinical treatment is still challenging. Translocation associated membrane protein 1 (TRAM1), an adapter protein, participates in a variety of transduction pathways and mediates the biological functions such as cell proliferation, activation, and differentiation. However, whether TRAM1 is involved in the pathogenesis of neuropathic pain is still unclear. In our study, we reported the role of TRAM1 in the maintenance of neuropathic pain induced by chronic constriction injury (CCI) on rats. By west...
Source: Journal of Molecular Neuroscience - October 18, 2018 Category: Neuroscience Source Type: research

Lentiviral ‑mediated inducible silencing of TLR4 attenuates neuropathic pain in a rat model of chronic constriction injury.
In conclusion, TLR4 may serve a significant role in neuropathy and the results of the present study provide an inducible lentivirus‑mediated siRNA against TLR4 that may serve as a potential novel strategy to be applied in gene therapy for NP in the future. PMID: 30365084 [PubMed - as supplied by publisher]
Source: Molecular Medicine Reports - October 27, 2018 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Inhibition of TREM1 reduces inflammation and oxidative stress after spinal cord injury (SCI) associated with HO-1 expressions
Publication date: January 2019Source: Biomedicine & Pharmacotherapy, Volume 109Author(s): Zhenhuan Li, Furong Wu, Dafeng Xu, Zhongzheng Zhi, Guanghui XuAbstractSpinal cord injury (SCI) is a devastating event, leading to the progression of chronic neuropathic pain syndrome. Triggering receptor expressed on myeloid cells 1 (TREM1) is an innate immune receptor expressed on neutrophils and monocytes/macrophages. TREM1 enhances inflammatory response in various models of diseases, but its significance in SCI remains unclear. In the present study, we attempted to explore the effects of TREM1 on the regulation of SCI. Spinal cord ...
Source: Biomedicine and Pharmacotherapy - November 27, 2018 Category: Drugs & Pharmacology Source Type: research

Downregulated spinal IRF8 and BDNF in NAC are involved in neuropathic pain-induced depression relief via pulsed radiofrequency on dorsal root ganglion in rat SNI model.
This study was designed to explore the effect of PRF on DRG on the neuropathic pain-induced depression in rats with spared nerve injury (SNI). Here, we found that PRF on DRG or intrathecal injection of the interferon regulatory factor 8 (IRF8) siRNA prevented the increase of mechanical allodynia and depression-like behaviors of rats after receiving SNI. Meanwhile, Western blot, immunohistochemistry, and RT-PCR revealed that PRF on DRG or intrathecal injection of IRF8 siRNA inhibited IRF8 overexpression in the spinal cord and brain-derived neurotrophic factor (BDNF) in NAc. These results suggest that neuropathic pain-induce...
Source: Brain Research Bulletin - January 9, 2019 Category: Neurology Authors: Fang X, Xu X, Lin X, Liu R Tags: Brain Res Bull Source Type: research

Interleukin-1 Receptor Associated Kinase 1 Mediates the Maintenance of Neuropathic Pain after Chronic Constriction Injury in Rats.
Abstract Neuropathic pain (NP) has complicated pathogenesis as it mainly involves a lesion or dysfunction of the somatosensory nervous system and its clinical treatment remains challenging. Chronic constriction injury (CCI) model is a widely used neuropathic pain model and involved in mechanisms including both nerve inflammatory and injury. Cytokines and their receptors play essential roles in the occurrence and persistence of neuropathic pain, but the underlying mechanisms have not well been understood. Therefore, Interleukin-1 receptor-associated kinase 1 (IRAK1) is chosen to explore the possible mechanisms of N...
Source: Neurochemical Research - March 10, 2019 Category: Neuroscience Authors: Yin D, Chen Y, Li Y, Lu R, Wang B, Zhu S, Fan B, Xu Z Tags: Neurochem Res Source Type: research