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Condition: Back Pain

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Total 191 results found since Jan 2013.

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

Intrathecal injection of phosphodiesterase 4B-specific siRNA attenuates neuropathic pain in rats with L5 spinal nerve ligation.
Authors: Ji Q, Di Y, He X, Liu Q, Liu J, Li W, Zhang L Abstract Phosphodiesterase 4 (PDE4) is an adenosine cyclic 3,5-monophosphate-specific degradative enzyme, which is closely associated with the inflammatory response. Among its four subtypes (A‑D), it remains unclear which one exerts suppressive effects on inflammation and reduces neuropathic pain. The present study aimed to examine the modulation of neuroinflammation by PDE4 subtypes in the spinal cord of a rat model of L5 spinal nerve ligation (SNL)‑induced neuropathic pain. The expression levels of PDE4A‑D were measured in the lumbar spinal cords of naÃ...
Source: Molecular Medicine Reports - December 29, 2015 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

JAB1 is Involved in Neuropathic Pain by Regulating JNK and NF-κB Activation After Chronic Constriction Injury.
This study aimed to investigate the possible involvement of JAB1. Here, employing a neuropathic pain model induced by chronic constriction injury (CCI) on rats, we reported the role of JAB1 in the maintenance of neuropathic pain. By western blot, we found that CCI markedly up-regulated JAB1 expression in the dorsal root ganglion (DRG) and spinal cord. Immunofluorescent assay demonstrated that JAB1 was extensively localized in IB4-, CGRP- and NF200-positive neurons in the injured L5 DRG, and mainly co-localized with NeuN in spinal cord. In addition, we showed that CCI induced phosphorylation of p65 and JNK in vivo. Intrathe...
Source: Neurochemical Research - December 23, 2015 Category: Neuroscience Authors: Chen Y, Chen X, Yu J, Xu X, Wei X, Gu X, Liu C, Zhang D, Xu Z Tags: Neurochem Res Source Type: research

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

Anti-cancer effect of bee venom on colon cancer cell growth by activation of death receptors and inhibition of nuclear factor kappa B.
Authors: Zheng J, Lee HL, Ham YW, Song HS, Song MJ, Hong JT Abstract Bee venom (BV) has been used as a traditional medicine to treat arthritis, rheumatism, back pain, cancerous tumors, and skin diseases. However, the effects of BV on the colon cancer and their action mechanisms have not been reported yet. We used cell viability assay and soft agar colony formation assay for testing cell viability, electro mobility shift assay for detecting DNA binding activity of nuclear factor kappa B (NF-κB) and Western blotting assay for detection of apoptosis regulatory proteins. We found that BV inhibited growth of colon canc...
Source: Oncotarget - November 14, 2015 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Down-regulation of astroglial glutamate transporter-1 in the locus coeruleus impairs pain-evoked endogenous analgesia in rats
Publication date: Available online 9 October 2015 Source:Neuroscience Letters Author(s): Masafumi Kimuram, Takashi Suto, James C. Eisenach, Ken-ichiro Hayashida Descending noradrenergic inhibition to the spinal cord from the locus coeruleus (LC) is an important endogenous pain-relief mechanism which can be activated by local glutamate signaling. Here we tested whether dysregulation of extracellular glutamate level in the LC induced by down-regulating astroglial glutamate transporter-1(GLT-1) impairs endogenous analgesia. In rats treated with repeated LC injections of GLT-1 selective or non-targeting small interfering...
Source: Neuroscience Letters - October 10, 2015 Category: Neuroscience Source Type: research

Tumor necrosis factor-mediated downregulation of spinal astrocytic connexin43 leads to increased glutamatergic neurotransmission and neuropathic pain in mice
Publication date: Available online 24 June 2015 Source:Brain, Behavior, and Immunity Author(s): Norimitsu Morioka , Fang Fang Zhang , Yoki Nakamura , Tomoya Kitamura , Kazue Hisaoka-Nakashima , Yoshihiro Nakata Spinal cord astrocytes are critical in the maintenance of neuropathic pain. Connexin 43 (Cx43) expressed on spinal dorsal horn astrocytes modulates synaptic neurotransmission, but its role in nociceptive transduction has yet to be fully elaborated. In mice, Cx43 is mainly expressed in astrocytes, not neurons or microglia, in the spinal dorsal horn. Hind paw mechanical hypersensitivity was observed beginning 3days ...
Source: Brain, Behavior, and Immunity - July 3, 2015 Category: Neurology Source Type: research

Tumor necrosis factor-mediated downregulation of spinal astrocytic connexin43 leads to increased glutamatergic neurotransmission and neuropathic pain in mice.
Abstract Spinal cord astrocytes are critical in the maintenance of neuropathic pain. Connexin 43 (Cx43) expressed on spinal dorsal horn astrocytes modulates synaptic neurotransmission, but its role in nociceptive transduction has yet to be fully elaborated. In mice, Cx43 is mainly expressed in astrocytes, not neurons or microglia, in the spinal dorsal horn. Hind paw mechanical hypersensitivity was observed beginning 3 days after partial sciatic nerve ligation (PSNL), but a persistent downregulation of astrocytic Cx43 in ipsilateral lumbar spinal dorsal horn was not observed until 7 days post-PSNL, suggesting that ...
Source: Brain, Behavior, and Immunity - June 23, 2015 Category: Neurology Authors: Morioka N, Zhang FF, Nakamura Y, Kitamura T, Hisaoka-Nakashima K, Nakata Y Tags: Brain Behav Immun Source Type: research

Epigenetic Control of Pannexin-1 Expression in Chronic Pain Neurobiology
In this study, we determined the epigenetic mechanism involved in increased Panx1 expression in the DRG after nerve injury. Spinal nerve ligation in rats significantly increased the mRNA and protein levels of Panx1 in the DRG but not in the spinal cord. Immunocytochemical labeling showed that Panx1 was primarily expressed in a subset of medium and large DRG neurons in control rats and that nerve injury markedly increased the number of Panx1-immunoreactive DRG neurons. Nerve injury significantly increased the enrichment of two activating histone marks (H3K4me2 and H3K9ac) and decreased the occupancy of two repressive histon...
Source: Journal of Biological Chemistry - June 4, 2015 Category: Chemistry Authors: Zhang, Y., Laumet, G., Chen, S.-R., Hittelman, W. N., Pan, H.-L. Tags: Molecular Bases of Disease Source Type: research

TCF4 Mediates the Maintenance of Neuropathic Pain Through Wnt/β-Catenin Signaling Following Peripheral Nerve Injury in Rats
Abstract Neuropathic pain is elicited after a serious disorder of the nervous system and is along with the neural damage. It is usually chronic and challenging to treat. Transcription factor 4 (TCF4) is a key transcription factor of Wnt signaling system. Recent studies have shown that TCF4 interacts with β-catenin in the Wnt signaling pathway and coactivates downstream target genes in diverse systems. However, it is not well elucidated in the pathogenesis of neuropathic pain. In the present study, we investigated the role of TCF4 in the maintenance of neuropathic pain after chronic constriction injury (CCI) in ra...
Source: Journal of Molecular Neuroscience - May 11, 2015 Category: Neuroscience Source Type: research

MicroRNA-146a-5p attenuates neuropathic pain via suppressing TRAF6 signaling in the spinal cord
In this study, we found that in cultured astrocytes, TNF-α, IL-1β, or lipopolysaccharides (LPSs) induced rapid TRAF6 upregulation and delayed miR-146a-5p upregulation. In addition, miR-146a-5p mimic blocked LPS-induced TRAF6 upregulation, as well as LPS-induced c-Jun N-terminal kinase (JNK) activation and chemokine CCL2 expression in astrocytes. Notably, LPS incubation with astrocytes enhanced the DNA binding activity of AP-1 to the promoters of mir-146a and ccl2. TRAF6 siRNA or JNK inhibitor SP600125 significantly reduced LPS-induced miR-146a-5p increase in astrocytes. In vivo, intrathecal injection of TNF-α or LPS inc...
Source: Brain, Behavior, and Immunity - May 7, 2015 Category: Neurology Source Type: research

MicroRNA-146a-5p attenuates neuropathic pain via suppressing TRAF6 signaling in the spinal cord.
In this study, we found that in cultured astrocytes, TNF-α, IL-1β, or lipopolysaccharides (LPSs) induced rapid TRAF6 upregulation and delayed miR-146a-5p upregulation. In addition, miR-146a-5p mimic blocked LPS-induced TRAF6 upregulation, as well as LPS-induced c-Jun N-terminal kinase (JNK) activation and chemokine CCL2 expression in astrocytes. Notably, LPS incubation with astrocytes enhanced the DNA binding activity of AP-1 to the promoters of mir-146a and ccl2. TRAF6 siRNA or JNK inhibitor SP600125 significantly reduced LPS-induced miR-146a-5p increase in astrocytes. In vivo, intrathecal injection of TNF-α or LPS inc...
Source: Brain, Behavior, and Immunity - May 5, 2015 Category: Neurology Authors: Lu Y, Cao L, Jiang BC, Yang T, Gao YJ Tags: Brain Behav Immun Source Type: research

Silencing Cytokines in-vivo with i-Fect
Knocking Down Cytokine to Study Pain ResponseWe have many unique applications published from researchers using our Transfection Kits in vitro and in vivo. Here researchers simultaneously 3 immune/inflammatory response cytokines in vivo: Byung Moon Choi, Soo Han Lee, Sang Mee An, Do Yang Park, Gwan Woo Lee, and Gyu-Jeong Noh. 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. Korean J Anesthesiol. 2015 Apr;68(2):159-169. English. Published online March 30, 2015. http://dx.doi.org/10.4097/kjae.2015.68.2.159.Protocol: RNAs w...
Source: siRNA and DsiRNA Transfection Efficiency - April 7, 2015 Category: Neuroscience Tags: allodynia analgesia Gene Expression Analysis Gene Silencing i-Fect IL-1B IL-6 inflammatory pain intrathecal delivery of siRNA TNF-alpha Transfection Kits Source Type: news

Local knockdown of the NaV1.6 sodium channel reduces pain behaviors, sensory neuron excitability, and sympathetic sprouting in rat models of neuropathic pain
In this study, we injected small inhibitory (si) RNA directed against the NaV1.6 sodium channel isoform into the DRG before SNL. This isoform can mediate high-frequency repetitive firing, like that seen in spontaneously active neurons. Local knockdown of NaV1.6 markedly reduced mechanical pain behaviors induced by SNL, reduced sympathetic sprouting into the ligated sensory ganglion, and blocked abnormal spontaneous activity and other measures of hyperexcitability in myelinated neurons in the ligated sensory ganglion. Immunohistochemical experiments showed that sympathetic sprouting preferentially targeted NaV1.6-positive n...
Source: Neuroscience - March 6, 2015 Category: Neuroscience Source Type: research

Intrathecal siRNA Against GPNMB Attenuates Nociception in a Rat Model of Neuropathic Pain
Abstract Neuropathic pain is characterized by hyperalgesia, allodynia, and spontaneous pain. Recent studies have shown that glycoprotein nonmetastatic melanoma B (GPNMB) plays a pivotal role in neuronal survival and neuroprotection. However, the role of GPNMB in neuropathic pain remains unknown. The aim of the present study was to assess the role of GPNMB in neuropathic pain. In cultured spinal cord neurons, we used two small interfering RNAs (siRNAs) targeting the complementary DNA (cDNA) sequence of rat GPNMB that had potent inhibitory effects on GPNMB, and siRNA1-GPNMB was selected for further in vivo study as...
Source: Journal of Molecular Neuroscience - January 23, 2015 Category: Neuroscience Source Type: research