• Journal of Korean Neurosurgical Society
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• v.64 no.6
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• pp.873-881
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• 2021

Objective : Peripheral nerve injuries occur mostly as a result of mechanical trauma. Due to the microvascular deterioration in peripheral nerve damage, it becomes challenging to remove free oxygen radicals. Gallic acid is a powerful antioxidant with anti-inflammatory effects and a free radical scavenger. The purpose of the study is to show that gallic acid contributes to the restorative effect in mechanical nerve damage, considering its antioxidant and anti-inflammatory effects. Methods : Thirty male Sprague Dawley albino mature rats were included in the study. Ten of them constituted the control group, 10 out of 20 rats for which sciatic nerve damage was caused, constituted the saline group, and 10 formed the gallic acid group. Post-treatment motor functions, histological, immunohistochemical, and biochemical parameters of the rats were evaluated. Results : Compared to the surgery+saline group, lower compound muscle action potential (CMAP) latency, higher CMAP amplitude, and higher inclined plane test values were found in the surgery+gallic acid group. Similarly, a higher nerve growth factor (NGF) percentage, a higher number of axons, and a lower percentage of fibrosis scores were observed in the surgery+gallic acid group. Finally, lower tissue malondialdehyde (MDA) and higher heat shock protein-70 (HSP-70) values were determined in the surgery+gallic acid group. Conclusion : Gallic acid positively affects peripheral nerve injury healing due to its anti-inflammatory and antioxidant effects. It has been thought that gallic acid can be used as a supportive treatment in peripheral nerve damage.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.2
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• pp.59-69
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• 2010

Impairment in spinal inhibition caused by quantitative alteration of GABAergic elements following peripheral nerve injury has been postulated to mediate neuropathic pain. In the present study, we tested whether neuropathic pain could be induced or reversed by pharmacologically modulating spinal GABAergic activity, and whether quantitative alteration of spinal GABAergic elements after peripheral nerve injury was related to the impairment of GABAergic inhibition or neuropathic pain. To these aims, we first analyzed the pain behaviors following the spinal administration of GABA antagonists ($1{\mu}g$ bicuculline/rat and $5{\mu}g$ phaclofen/rat), agonists ($1{\mu}g$ muscimol/rat and $0.5{\mu}g$ baclofen/rat) or GABA transporter (GAT) inhibitors ($20{\mu}g$ NNC-711/rat and $1{\mu}g$ SNAP-5114/rat) into naive or neuropathic animals. Then, using Western blotting, PCR or immunohistochemistry, we compared the quantities of spinal GABA, its synthesizing enzymes (GAD65, 67) and its receptors (GABAA and GABAB) and transporters (GAT-1, and -3) between two groups of rats with different severity of neuropathic pain following partial injury of tail-innervating nerves; the allodynic and non-allodynic groups. Intrathecal administration of GABA antagonists markedly lowered tail-withdrawal threshold in naive animals, and GABA agonists or GAT inhibitors significantly attenuated neuropathic pain in nerve-injured animals. However, any quantitative changes in spinal GABAergic elements were not observed in both the allodynic and non-allodynic groups. These results suggest that although the impairment in spinal GABAergic inhibition may play a role in mediation of neuropathic pain, it is not accomplished by the quantitative change in spinal elements for GABAergic inhibition and therefore these elements are not related to the generation of neuropathic pain following peripheral nerve injury.

• Journal of Korean Neurosurgical Society
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• v.50 no.2
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• pp.109-113
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• 2011

Objective : Peripheral neuropathy is characterized by hyperalgesia, spontaneous burning pain, and allodynia. The purpose of this study was to investigate the effect of rolipram, a phosphodiesterase-4-specific inhibitor, in a segmental spinal nerve ligation model in rats. Methods : Both the L5 and L6 spinal nerves of the left side of the rats were ligated. Phosphodiesterase-4 inhibitor (rolipram) and saline (vehicle) were administered intraperitoneally. We measured mechanical allodynia using von Frey filaments and a nerve conduction study. Results : The mechanical allodynia, which began to manifest on the first day, peaked within 2 days. Multiple intraperitoneal injections of rolipram ameliorated the mechanical allodynia. Furthermore, an intraperitoneal administration of rolipram improved the development of pain behavior and nerve conduction velocity. Conclusion : This study suggests that the phosphodiesterase-4 inhibitor, rolipram, alleviates mechanical allodynia induced by segmental spinal nerve ligation in rats. This finding may have clinical implications.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.3
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• pp.251-262
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• 1997

Peripheral nerve injury sometimes leads to neuropathic pain and depletion of calcitonin gene related-peptide (CGRP) and substance P (SP) in the spinal cord. However, the pathophysiological mechanisms for depletion of CGRP and SP following the neurorathic injury are still unknown. This study was performed to see whether the distribution of immunoreactivity for CGRP and SP in the superficial dorsal horn and dorsal root ganglia(DRG) was related to the distance between the DRG and injury site. To this aim, we compared two groups of rats; one group was subjected to unilateral inferior and superior caudal trunk transections at the level between the S3 and S4 spinal nerves (S34 group) and the other group at the levels between the S1 and S2, between S2 and S3 and between S3 and S4 spinal nerve (S123 group). The transections in both groups equally eliminated the inputs from the tail to the S1-3 DRG, but the distance from the S1/S2 DRG to the injury site was different between the two groups. Immunostaining with SP and CGRP antibody was done in the S1-S3 spinal cord and DRG of the two groups 1 and 12 weeks after the injury. The results obtained are as follows: 1. The immunoreactivity for CGRP and SP in the ipsilateral superficial dorsal horn and DRG decreased 1 and 12 weeks after neuropathic nerve injury. 2. The immunoreactive area of SP and CGRP in the S1 dorsal horn was smaller in the S123 group than in the S34 group, whereas that in the S3 dorsal horn was not significantly different between the two groups. The number of SP-immunoreactive DRG cells decreased on the neuropathic side as compared to the sham group's in all DRGs of experimental groups except the S1 DRG of the S34 group. These results suggest that the amounts of SP and CGRP in the dorsal horn and DRG following neuropathic injury inversely decrease according to the distance between the DRG and injury site.

• Journal of Korean Biological Nursing Science
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• v.10 no.1
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• pp.88-95
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• 2008

Purpose: The purpose of this study was to examine the effect of neuropathic pain by peripheral nerve injury on mass and Type I and II fiber cross-sectional areas on hindlimb muscles of the neuropathic pain model rat. Method: Adult male Sprague-Dawley rats (body weight 200-220 g) were assigned to one of two groups: a neuropathic pain group (n=7) that had a ligation of the left L5 spinal nerve, a control group (n=5), a naive rat without any procedures. Withdrawal threshold, activity, body weight and food intake were measured daily. At 8 days after neuropathic pain, all rats were anesthetized and the soleus and plantaris muscles were dissected from the both hindlimbs. Body weight, food intake, muscle weight and Type I and II fiber cross-sectional area of the dissected muscles were determined. Result: The neuropathic pain group showed a significant decreases (p<.05) as compared with the control rats, in diet intake, body weight, muscle weight and Type II fiber cross-sectional area of the left (affected side) soleus and plantaris muscles, and the right (unaffected side) muscle weight of plantaris and Type II fiber cross-sectional area of the soleus muscle. Conclusion: The hindlimb muscle atrophy occurs in both affected and unaffected side due to neuropathic pain by the peripheral nerve injury. The hindlimb muscle atrophy of the affected side is more pronounced than that of the unaffected side.

• The Korean Journal of Pain
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• v.28 no.4
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• pp.287-289
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• 2015

Brachial plexus block (BPB) under ultrasound guidance has come to be widely used. However, nerve injury has been reported following ultrasound-guided BPB. We hypothesized that BPB under ultrasound guidance in conjunction with real-time electrical nerve stimulation would help us prevent nerve injury and do more successful procedure. Here, we report the successful induction and maintenance of ultrasound-guided BPB and the achievement of good peri- and postoperative pain control using a conductive catheter, the EpiStim$^{(R)}$.

• Korean Journal of Veterinary Research
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• v.44 no.4
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• pp.483-486
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• 2004

The expression of nestin and vimentin in the spinal nerve roots of rats with experimental autoimmune encephalomyelitis (EAE) was studied to ascertain whether Schwann cells in the peripheral nerves respond to acute central nervous system autoimmune injury. Immunohistochemistry demonstrated that nestin was constitutively expressed in the dorsal roots of spinal nerves in control rats; its expression was enhanced in the spinal nerve roots of rats with EAE. Vimentin expression was weak in control rat spinal nerve roots, and it was increased in the dorsal roots of rats with EAE. It is postulated that normal animals have multipotent progenitor cells that constitutively express nestin and vimentin in the spinal nerve roots. In response to an injury of the central nervous system, these multipotent Schwann cells are activated in the spinal nerve roots through the expression of the intermediate filament proteins vimentin and nestin.

• Proceedings of the KOSOMBE Conference
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• v.1996 no.11
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• pp.99-102
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• 1996

The ultimate object of FES is on the recovering function of body and shape demaged from desease or injury to original state. On this study, object is recovering of gait function of the disabled who, especially, have gait disturbance. Paralyzed muscle from the central nerve disable, if peripheral nerves which be in the lower part of the harmed are activated, muscle contraction is possible. The traumatic trouble, peripheral nerves aren't connected to a central nerve but origin of peripheral nerve cells which are in the lower part of the harmed are alive, react on stimulation. We design 4-channel stimulator, being based on standard stimuli pattern. stimulator is manufactured with compact size and light weight to portable.

• International Journal of Oral Biology
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• v.31 no.3
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• pp.87-92
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• 2006

Schwann cells play an important role in peripheral nerve regeneration. Upon nerve injury, Schwann cells are activated and produce various proinflammatory mediators including IL-6, LIF and MCP-1, which result in the recruitment of macrophages and phagocytosis of myelin debris. However, it is unclear how the nerve injury induces Schwann cell activation. Recently, it was reported that necrotic cells induce immune cell activation via toll-like receptors (TLRs). This suggests that the TLRs expressed on Schwann cells may recognize nerve damage by binding to the endogenous ligands secreted by the damaged nerve, thereby inducing Schwann cell activation. To explore the possibility, we stimulated iSC, a rat Schwann cell line, with damaged neuronal cell extracts (DNCE). The stimulation of iSC with DNCE induced the expression of various inflammatory mediators including IL-6, LIF, MCP-1 and iNOS. Studies on the signaling pathway indicate that $NF-{\kappa}B$, p38 and JNK activation are required for the DNCE-induced inflammatory gene expression. Furthermore, treatment of either anti-TLR3 neutralizing antibody or ribonuclease inhibited the DNCE-induced proinflammatory gene expression in iSC. In summary, these results suggest that damaged neuronal cells induce inflammatory Schwann cell activation via TLR3, which might be involved in the Wallerian degeneration after a peripheral nerve injury.

• Journal of Dental Rehabilitation and Applied Science
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• v.28 no.2
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• pp.171-178
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• 2012

Botulinum toxin type A (BoNT-A) has been applied successfully to treat chronic migraine, dystonia, spasticity and temporomandubular disorders(TMDs) as well as frontal wrinkle and glabella wrinkle. Recently it has been reported that BoNT-A, reversibly blocks presynaptic acetylcholine release, also inhibits the release of substance P, CGRP(calcitonin gene related peptide) and glutamate related to peripheral sensitization and neurogenic inflammation in sensory nerve, In this study we reviewed animal nerve injury model such as rat and rabbit and identify the analgesic effect and mechanism of nerve injury pain after dental treatment.