• Korean Journal of Acupuncture
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• 제30권1호
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• pp.73-80
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• 2013

Objectives : LI11 has been known to suppress epileptic seizure. Using an mouse epilepsy model, we investigated whether acupuncture stimulation at LI11 can suppress kainic acid(KA)-induced epileptic seizure and apoptosis in the mouse hippocampus. Methods : Eight-week-old male C57/BL6 mice(20~25 g) were given acupuncture at LI11 or ST36 once a day for 3 days. After the last acupuncture stimulations, KA(30 mg/kg) was injected intraperitoneally and the degree of seizure was observed for 90 minutes. Twenty-four hours after KA administration, mice were sacrificed and the neural cell death, astrocyte activation and caspase-3 expression in their hippocampi were investigated. Results : Acupuncture stimulation at LI11 suppressed KA-induced epileptic seizure, neuronal cell death, astrocyte activation and caspase-3 expression. Conclusions : Acupuncture stimulation at LI11 decreases the KA-induced epileptic seizure and protects hippocampal cell death via regulating astrocyte activation and caspase-3 expression.

• Journal of Ginseng Research
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• 제40권3호
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• pp.211-219
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• 2016

Background: Panax ginseng root is used in traditional oriental medicine for human health. Its main active components such as saponins and polysaccharides have been widely evaluated for treating diseases, but secondary active components such as oligosaccharides have been rarely studied. This study aimed to assess the impact of water-soluble ginseng oligosaccharides (WGOS), which were isolated from the warm-water extract of Panax ginseng root, on scopolamine-induced cognitive impairment in mice and its antineuroinflammatory mechanisms. Methods: We investigated the impact of WGOS on scopolamine-induced cognitive impairment in mice by using Morris water maze and novel object recognition task. We also analyzed the impact of WGOS on scopolamine-induced inflammatory response (e.g., the hyperexpression of proinflammatory cytokines IL-$1{\beta}$ and IL-6 and astrocyte activation) by quantitative real-time polymerase chain reaction and glial fibrillary acid protein (GFAP) immunohistochemical staining. Results: WGOS pretreatment protected against scopolamine-induced learning and memory deficits in the Morris water maze and in the novel object recognition task. Furthermore, WGOS pretreatment downregulated scopolamine-induced hyperexpression of proinflammatory cytokines interleukin (IL)-$1{\beta}$ and IL-6 mRNA and astrocyte activation in the hippocampus. These results indicate that WGOS can protect against scopolamine-induced alterations in learning and memory and inflammatory response. Conclusion: Our data suggest that WGOS may be beneficial as a medicine or functional food supplement to treat disorders with cognitive deficits and increased inflammation.

• 한국체육학회지인문사회과학편
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• 제58권4호
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• pp.481-492
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• 2019

본 연구는 12주간의 트레드밀 운동이 노화 흰쥐 소뇌의 성상세포 활성과 퍼킨제 세포 발현 및 운동기능 변화에 미치는 영향에 대해 알아보았다. Sprague-Dawley(SD) 흰쥐를 실험처치에 따라 (1)젊은 통제집단 (Young Control Group; YCG; 3months aged; n=10), (2) 노화 통제집단 (Old Control Group; OCG; 24months aged; n=10), (3) 노화 운동집단 (Old Exercise Group; OEG; 24months aged; n=10)으로 구분한 후 OEG는 트레드밀 운동을 시간과 강도를 점증적으로 증가하여 12주간, 주 5회 실시하였다. 실험결과 rota-rod 검사에서 운동기능이 OCG에 비해 OEG에서 증가하는 것으로 나타났으며(p<.05) 그 수준은 YCG와 유사한 것으로 나타났다. calbindin-양성 퍼킨제 세포의 발현도 OCG에 비해 OEG의 소뇌 충부에서 증가하였으며(p<.05), 그 수준은 YCG와 유사하였다. GFAP-, NMDAR-양성세포의 발현도 OEG에서 증가하였다(각각 p<.001). GFAP, GLAST 단백질 수준은 OCG에 비해 OEG에서 증가하였으며(p<.05, p<.001) 그 수준은 YCG와 유사하였다. BDNF, NGF 수준은 YCG에서 가장 높았으며 OCG에 비해 OEG에서 증가하는 것으로 나타났다(p<.001, p<.05). 이상의 결과를 종합하면 규칙적인 운동은 성상세포의 활성을 향상시킬 뿐만 아니라 신경영양인자의 증가를 통하여 소뇌의 퍼킨제 세포 발현과 운동기능을 개선시키는 것으로 판단된다.

• The Korean Journal of Pain
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• 제36권1호
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• pp.51-59
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• 2023

Background: This study investigated the effect of an excess and a deficit of spinal 5-hydroxytryptamine (5-HT) on the mechanical allodynia and neuroglia activation in a rodent pain model of carrageenan inflammation. Methods: Male Sprague-Dawley rats were implanted with an intrathecal (i.t.) catheter to administer the drug. To induce an excess or deficit of 5-HT in the spinal cord, animals were given either three i.t. 5-HT injections at 24-hour intervals or a single i.t. injection of 5,7-dihydroxytryptamine (5,7-DHT) before carrageenan inflammation. Mechanical allodynia was measured using the von Frey test for 0-4 hours (early phase) and 24-28 hours (late phase) after carrageenan injection. The changes in the activation of microglia and astrocyte were examined using immunofluorescence of the dorsal horn of the lumbar spinal cord. Results: Both an excess and a deficit of spinal 5-HT had no or a minimal effect on the intensity of mechanical allodynia during the early phase but prevented the attenuation of mechanical allodynia during the late phase, which was observed in animals not treated with i.t. 5-HT or 5,7-DHT. Animals with an excess or deficit of 5-HT showed stronger activation of microglia, but not astrocyte, during the early and late phases, than did normal animals. Conclusions: Imbalance in the descending 5-HT pathway in the spinal cord could aggravate the mechanical allodynia and enhance the activation of microglia, suggesting that the spinal 5-HT pathway plays an essential role in maintaining the nociceptive processing in balance between facilitation and inhibition in inflammatory pain caused by carrageenan inflammation.

• Journal of Korean Neurosurgical Society
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• 제49권2호
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• pp.83-91
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• 2011

Objective : Minocycline, a second-generation tetracycline-class antibiotic, has been well established to exert a neuroprotective effect in animal models and neurodegenerative disease through the inhibition of microglia. Here, we investigated the effects of minocycline on motor recovery and neuropathic pain in a rat model of spinal cord injury. Methods : To simulate spinal cord injury, the rats' spinal cords were hemisected at the 10th thoracic level (T10). Minocycline was injected intraperitoneally, and was administered 30 minutes prior surgery and every second postoperative day until sacrifice 28 days after surgery. Motor recovery was assessed via the Basso-Beattie-Bresnahan test Mechanical hyperalgesia was measured throughout the 28-day post -operative course via the von Frey test Microglial and astrocyte activation was assessed by immunohistochemical staining for ionized calcium binding adaptor molecule 1 (lba1) and glial fibrillary acidic protein (GFAP) at two sites: at the level of hemisection and at the 5th lumbar level (L5). Results : In rats, spinal cord hemisection reduced locomotor function and induced a mechanical hyperalgesia of the ipsilateral hind limb. The expression of lba1 and GFAP was also increased in the dorsal and ventral horns of the spinal cord at the site of hemisection and at the L5 level. Intraperitoneal injection of minocycline facilitated overall motor recovery and attenuated mechanical hyperalgesia. The expression of lba1 and GFAP in the spinal cord was also reduced in rats treated with minocycline. Conclusion : By inhibiting microglia and astrocyte activation, minocycline may facilitate motor recovery and attenuate mechanical hyperalgesia in individuals with spinal cord injuries.

• 동의생리병리학회지
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• 제23권2호
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• pp.374-380
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• 2009

Samryungbaikchul-san(SRBCS) has been used in oriental medicine for the treatments of gastrointestinal and neurological disorders. Here, potential protective function of SRBCS was investigated in neural tissues in Alzheimer's disease(AD) mouse model. In primary cultured cells from the spinal cord of newborn rats, treatment of ${\beta}$-amyloid peptide elevated cell counts positive to glial fibrillary acidic protein(GFAP) or caspase 3 immunoreactivity, but the co-treatment of SRBCS reduced positive cell counts. In vivo administration of scopolamine, an inhibitor of muscarinic receptor, resulted in increases in the number of glial fibrillary acidic protein(GFAP) and caspase 3-positive cells in hippocampal subfields, which was then decreased by the treatment of SRBCS or acetylcholinesterase inhibitor galathamine. The present data suggest that SRBCS may play a protective role in damaged neural tissues caused by scopolamine treatments in mice.

• Korean Journal of Acupuncture
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• 제29권3호
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• pp.396-405
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• 2012

Objectives : To confirm whether acupuncture can suppress the degree of seizure and the activation of astrocytes in hippocampi using kainic acid(KA)-induced epilepsy mouse model. Methods : 8 weeks C57BL/6 mice(20~25 g) were given acupuncture once a day at acupoint HT8(Shaofu) bilaterally during 2 days before KA injection. After an intraperitoneal injection of 30 mg/kg KA, acupuncture treatment was subsequently administered once more(total 3 times), and the degree of seizure was observed for 120 min. The neuronal cell death, pERK expression, and astrocyte activation confirmed 1 hour and 24 hours after KA injection. Results : Acupuncture treatment at HT8 suppressed KA-induced epileptic seizure. One hour after KA injection, the pERK expression was increased, which was reduced by the acupuncture treatment. Twenty four hours after injection, the treatment decreased the KA-induced neuronal cell death, the interleukin-$1{\beta}$ expression and the astrocyte activation in the CA3 region of the mouse hippocampus. Conclusions : Acupuncture treatment at HT8 decreases the KA-induced epileptic seizure, the neural cell inflammation and death.

• 한국식물생명공학회:학술대회논문집
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• 한국식물생명공학회 2004년도 생명공학 실용화를 위한 비젼
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• pp.74-79
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• 2004

Little is known about the effect of epigallocatechin-3 gallate (ESCG), a major constituent of green tea, on the expression of cyclooxygenase (COX)-2. Here, we studied the role of phospholipase D (PLD) isozymes in EGCG-induced COX-2 expression. Stimulation of human astrocytoma cells (U87) with EGCG induced formation of phosphatidylbutanol, a specific product of PLD activity, and synthesis of COX-2protein and its product, prostaglandin $E_2$ ($PGE_2$). Pretreatment of cells with 1-butanol, but not 3-butanol, suppressed EGCG-induced COX-2 expression and $PGE_2$ synthesis. Furthermore, evidence that PLD was involved in EGCG-induced COX-2 expression w3s provided by the observations that COX-2 expression was stimulated by over-expression of PLD1 or PLD2 isozymes and treatment with phosphatidic acid(PA), and that prevention of PA dephosphorylation by 1-propranolol significantly potentiated COX-2expression Induced by EGCG. EGCG induced activation of p38 mitogen-activated protein kinase (p38MAPK), and specific Inhibition of p38 MAPK dramatically abolished EGCG-Induced PLD activation, COX-2 expression, and $PGE_2$ formation. Moreover, protein kinase C (PKC) inhibition suppressed EGCG-induced p38 MAPK activation, COX-2 expression, and $PGE_2$ accumulation. The same pathways as those obtained in the astrocytoma cells were active in primary rat astrocytes, suggesting the relevance of the findings. Collectively, our results demonstrate for the first time that PLD isozymes mediate EGCG-induced COX-2 expression through PKC and p38 in immortalized astroglial line and normal astrocyte cells.

• International Journal of Oral Biology
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• 제40권2호
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• pp.71-77
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• 2015

The activation of glial cells in the spinal cord has been contribute to the initiation and maintenance of pain facilitation induced by peripheral inflammation and nerve injury. The present study investigated effects of botulinum toxin type A (BoNT-A), injected subcutaneously or intracisternally, on the expression of microglia and astrocytes in rats. Complete Freund's Adjuvant (CFA)-induced inflammation was employed as an orofacial chronic inflammatory pain model. A subcutaneous injection of $40{\mu}L$ CFA into the vibrissa pad was performed under 3% isoflurane anesthesia in SD rats. Immunohistochemical analysis for changes in Iba1 (a microglia marker) and GFAP (an astrocyte marker), were performed 5 days after CFA injection. Subcutaneous injection of CFA produced increases in Iba1 and GFAP expression, in the ipsilateral superficial lamia I and II in the medullary dorsal horn of rats. Subcutaneous treatment with BoNT-A attenuated the up-regulation of Iba1 and GFAP expressions induced by CFA injection. Moreover, intracisternal injection of BoNT-A also attenuated the up-regulated Iba1 and GFAP expressions. These results suggest that the anti-nociceptive action of BoNT-A is mediated by modulation activation of glial cells, including microglia and astrocyte.

• 운동영양학회지
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• 제16권2호
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• pp.73-84
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• 2012

Thyroid hormones are important for the development of the brain including the cerebellum. In the present study, we investigated the effect of treadmill exercise on the survival of Purkinje neurons and the activation of astrocytes in the cerebellar vermis of hypothyroidism-induced rat pups. On the day of perinatal 14, pregnant rats were divided into two groups (n = 5 in each group): the pregnant control group and the pregnantmethimazole (MMI)-treated group. For the induction of hypothyroidism in the rat pups, MMI was added to the drinking water (0.02% wt/vol), from the day of perinatal 14 to postnatal 49. After delivery, male rat pups born from the pregnant control group were assigned to the control group. Male rat pups born from the MMI-treated group were divided into the hypothyroidism-induction group, the hypothyroidism-induction with treadmill exercise group, and the hypothyroidism-induction with thyroxine (T4) treatment group (n = 10 in each group). The rat pups in the exercise group were forced to run on a treadmill for 30 min once a day for 4 weeks, starting on postnatal day 22. In the hypothyroidism-induced rat pups, motor coordination was reduced and Purkinje cell death and reactive astrocytes in the cerebellar vermis were increased. Treadmill exercise enhanced motor coordination, increased the survival of Purkinje neurons, down-regulated reactive astrocytes, and enhanced brain-derived neurotrophic factor (BDNF) and receptor tyrosine kinase B (TrkB) expressions in the hypothyroidism-induced rat pups. These results suggest that treadmill exercise has beneficial effects in terms of protecting against thyroid dysfunction by increasing T3 and T4 and the related protein, BDNF, as well as TrkB, inhibition on astrocyte activation and the reduction of Purkinje cell loss regarding the cerebellum in hypothyroidism rat pups.