• Title/Summary/Keyword: 6-OHDA

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The Effect of the Swimming Exercise by Load on Concentration of BDNF in Serum and Behavioral Change of CNS Injury in the Rats (부하유무에 따른 수영운동이 중추신경계 손상 흰쥐의 혈청 BDNF 농도 및 행동변화에 미치는 영향)

  • Ha, Mi-Sook;Hyong, In-Hyouk
    • The Journal of the Korea Contents Association
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    • v.9 no.12
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    • pp.391-399
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    • 2009
  • The purposes of the present investigation was to evaluate the effects of loaded and unloaded swimming stimulation after central nerve system injury in the rats. SCI model rats were damaged in L1-L2 injected with 6-OHDA. The twenty one Sprague-Dawley adult male rats weights($200\pm10g$) were randomly divided into control group and 2 swimming groups and then swimming groups divided into 15 minute unloaded swimming group and 15 minute loaded swimming group by swimming intensity. Behavioral Change was evaluated by the BBB(Basso, Brestti, Brenahan) scales test and the maximal angles of the inclined board on which the rat could maintain its intial position for the progressive locomotor recovery. Using enzyme-linked immunosolbent assays(ELISA), we measured concentrations of brain-delived growth factor(BDNF) in serum after swimming. There was significant change of BBB scores in control group as compared to unloaded swimming group and loaded swimming group(p<.05), and unloaded swimming group were significantly higher than loaded swimming group(p<.05). The maximal angles of the inclined plane test were higher in the unloaded swimming group and loaded swimming group than the control group(p<.05), and loaded swimming group were significantly lower than unloaded swimming group(p<.05). There were singnificant difference of concentration of BDNF in serum change in each group(p<.05). The results suggest that swimming applied from the early phase after spinal cord injury may be beneficial in the early recovery of motor function.

The Effect of Electroacupuncture on Concentration and Activity of CK, ALP, and IgG in Serum and Central Nervous System of Rats (전침자극이 중추신경계 손상 흰쥐에서 CK, ALP, IgG 효소활성도에 미치는 영향)

  • Ha, Mi-Sook;Park, Rae-Joon
    • The Journal of Korean Physical Therapy
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    • v.22 no.2
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    • pp.47-53
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    • 2010
  • Purpose: This study investigated the effect of electroacupuncture stimulation on changes in blood biochemistry in spinal cord injury (SCI) rats whose cords were damaged by 6-hydroxydopamine (6-OHDA). Methods: Twenty-one Sprague-Dawley adult male rats were assigned to one of three groups: normal (n=7), control (n=7) and experimental group (n=7). The experimental group received electroacupuncture (Es-160, ITO, Japan) for 15 minutes in the form of low frequency (2 Hz) stimulation to the zusanli point. After treatment, we observed motor behavior recovery using the inclined plane test. We also measured serum and CNS concentrations and activities of enzymes including creatine kinase (CK), alkaline phosphatase (ALP), and Immunoglobulin G (IgG). Statistical analysis was done using one-way analysis of variance (ANOVA). Results: Concentrations of CK, ALP and IgG were lower in the experimental group than in the control group. Functional recovery was evaluated by the maximal angle of the inclined board on which rats could maintain their initial position. This allowed us to monitor progressive locomotor recovery. The maximal angles of the inclined plane test were higher in the experimental group than in the control group (p<0.05). Conclusion: The results of this study showed that electroacupuncture to the zusanli point has a therapeutic effect on functional recovery after SCI.

Effect of Decreased Locomotor Activity on Hindlimb Muscles in a Rat Model of Parkinson's Disease (파킨슨병 모델 쥐에서 보행활동저하가 뒷다리근에 미치는 영향)

  • Kim, Yong-Bum;Choe, Myoung-Ae
    • Journal of Korean Academy of Nursing
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    • v.40 no.4
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    • pp.580-588
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    • 2010
  • Purpose: The purpose of this study was to examine effects of decreased locomotor activity on mass, Type I and II fiber cross-sectional areas of ipsilateral and contralateral hindlimb muscles 21 days after establishing the Parkinson's disease rat model. Methods: The rat model was established by direct injection of 6-hydroxydopamine (6-OHDA, 50 ${mu}g$) into the left substantia nigra after stereotaxic surgery. Adult male Sprague-Dawley rats were assigned to one of two groups; the Parkinson's disease group (PD; n=17) and a sham group (S; n=8). Locomotor activity was assessed before and 21 days after the experiment. At 22 days after establishing the rat model, all rats were anesthetized and soleus and plantaris muscles were dissected from both ipsilateral and contralateral sides. The brain was dissected to identify dopaminergic neuronal death of substantia nigra in the PD group. Results: The PD group at 21 days after establishing the Parkinson's disease rat model showed significant decrease in locomotor activity compared with the S group. Weights and Type I and II fiber cross-sectional areas of the contralateral soleus muscle of the PD group were significantly lower than those of the S group. Conclusion: Contralateral soleus muscle atrophy occurs 21 days after establishing the Parkinson's disease rat model.

The Effects of Aerobic Exercise on Electrolytes Concentration after Spinal Cord Injured Rats (유산소운동이 척수손상 흰쥐의 전해질 농도에 미치는 영향)

  • Ha, Mi-Sook;Park, Rae-Joon
    • Journal of the Korean Society of Physical Medicine
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    • v.4 no.4
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    • pp.215-220
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    • 2009
  • Purpose:This study was to analyze the electrolyte such as blood Na+, K+, Ca2+ of aerobic exercise on spinal cord injured rats. Methods:SCI model rats were damaged in L1-L2 injected with 6-hydroxydopamine(6-OHDA). For this study went on classifying the control group without aerobic exercise, experimental group with aerobic exercise. Experimental groups were applied as swimming for 15minutes. Results:The results of this study were follows. 1) The body weight of the experimental group increased significantly after aerobic exercise(p<.05). 2) In the case of sodium(has been decreased significantly after 2 weeks(p<.05). 3) In the case of potassium has been increased significantly after 2 weeks(p<.05). 4) In the case of calcium has been increased significantly after 2 weeks(p<.05). Conclusion:Aerobic exercise were positive effect in body weight and electrolyte of the spinal cord injury. Continued swimming exercise can be recommended as an effective intervention for the spinal cord injury.

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Improvement of Motor Behavior of Parkinson′s Disease Animal Model by Nurr1-Transfected Human Embryonic Stem Cells.

  • Lee, Chang-Hyun;Cho, Hwang-Yoon;Kil, Kwang-Soo;Lee, Gun-Soup;Yoon, Ji-Yeon;Lee, Young-Jae;Kim, Eun-Young;Park, Se-Pill;Lim, Jin-Ho
    • Proceedings of the Korean Society of Developmental Biology Conference
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    • 2003.10a
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    • pp.103-103
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    • 2003
  • The purpose of this study is to evaluate an efficacy of in vitro differentiated human embryonic stem (hES, MB03) cells expressing Nurr1 in relief of symptomatic motor behavior of Parkinson's disease (PD) animal models MB03 was genetically modified to express Nurr1 protein and was induced to differentiate according to 2-/4+ protocol using retinoic acid and ascorbic acid. The differentiation-induced cells were selected for 10 to 20 days thereafter in N2 medium. Upon selection, cells expressing GFAP, TH, or NF200 were 38.8%, 11%, and 20.5%, respectively. in order to examine therapeutic effects of the differentiated cells in PD animal model, rats were unilaterally lesioned by administration of 6-kydroxydopamine HCI (6-OHDA) into medial forebrain region (MFB, AP -4.4 mm, ML 1.2 mm, DV 78 mm with incision bar set at -2.4 mm), as a reference to bregma and the surface of the skull. Confirmation of successful lesion by apomorphine-induced rotational behavior, differentiated cells were transplanted into the striatum (AP 1.0, ML 3.5, DV -5.0; AP 0.6, ML 2.5, DV -4.5). Improvements of asymmetric motor behavior by the transplantation were examined every two weeks after the surgery. In two weeks, numbers of rotation by the experimental rats were $-14.8 \pm 33.9%$ (P<0.05) of the number before transplantation, however, the ratio increased slightly to $13.6 \pm 56.3%$ in six weeks. In contrast, the ratio of sham-grafted animals ranged from 112.3+8.5% to 139.2+28.9% during the examination. Immunohistochemical studies further confirmed the presence, survival, migration, and expression of TH of the transplanted human cells.

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Review of the Antioxidant Effect of Herbal Material in In Vivo Parkinson's Disease Models (파킨슨병 in vivo 모델에서 한약재 및 기능성 식품의 항산화 효과에 대한 고찰)

  • Lee, Gi-hyang;Jeon, Sang-woo;Jeong, Min-jeong;Kim, Hong-jun;Jang, In-soo
    • The Journal of Internal Korean Medicine
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    • v.41 no.6
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    • pp.993-1014
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    • 2020
  • Objective: Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease. Antioxidant stress and inflammatory reactions are important causes of neurodegenerative diseases and are major causes of PD. Many animal experiments have been aimed at treating PD using the antioxidant effects of various traditional medicines and dietary supplements. This review reports the research investigating the antioxidant effects of herbs in in vivo PD models. Methods: The study consisted of a database search for articles related to PD and herbal treatments using the OASIS, NDSL, KTKP, Korean KISS, PubMed, Science Direct, CNKI, Wanfang, and J-STAGE databases. The search period was limited from the start of the search engine application to November 14, 2019. Studies were selected to confirm the antioxidant effects of herbal medicines in an in vivo PD model. Results: Eighty-two studies were summarized for plant species, extracts (or compounds), animal models, neurotoxins, and functional results. The most frequently used herbal materials were Bacopa monnieri, Camellia sinensis, Centella asiatica, and Withania somnifera. MPTP and 6-OHDA were the most commonly used neurotoxins for inducing PD. Most studies confirmed an increased expression and activation of antioxidant enzymes and a decrease in oxidative stress. Herbal materials showed their antioxidant effects regardless of the order of treatment and confirmed their possible use as treatments for the prevention and treatment of neurodegeneration. Conclusion: Many herbal medicines have antioxidant effects and are likely to be effective in delaying neurodegenerative damage by inhibiting or reducing oxidative stress by expression of antioxidant enzymes.

Neuroglial Reaction in the Substantia Nigra and Striatum of 6-Hydroxydopamine Induced Parkinson's Disease Rat Model (흰쥐 흑질내 수산화도파민 주입으로 유도된 파킨슨병 모델에서 흑질과 선조체의 신경교세포 반응)

  • Yang, Kyung Won;Sung, Jae Hoon;Kim, Moon Chan;Lee, Moon Yong;Lee, Sang Won;Choi, Seung Jin;Park, Choon Keun;Kang, Joon Ki
    • Journal of Korean Neurosurgical Society
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    • v.30 no.6
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    • pp.688-698
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    • 2001
  • Objectives : Parkinson's disease is a well-known neurodegenerative disease characterized by dopaminergic cell death in the substantia nigra. The reactive gliosis by activated astrocytes and microglias is no more regarded as a simple sequel of neuronal cell death. Microglial activation takes place in a stereotypic pattern with graded morphologic and functional(resting, activated and phagocytic) changes. In Parkinson's disease animal model, the degree of microglial activation along the nigro-striatal dopaminergic tract has not been studied intensively. The purpose of this study was to elucidate the characteristics of microglial reaction and to grade its degree of activation at substantia nigra and corpus striatum using 6-hydroxydopamine induced rat model of Parkinson's disease. Methods : Using Sprague-Dawley rat, parkinsonian model was made by 6-hydroxydopamine(OHDA) induced destruction of medial and lateral substantia nigra(SN). The rat was sacrificed 3-, 5-, 7-, 14- and 21-day-after operation. For control group, we injected saline with same manner and sacrificed 3-day after operation. With immunohistochemistry, we examined dopaminergic neuronal cells and microglial expression using tyrosine hydroxylase (TH) and OX-42 antibodies, respectively. Also we performed in situ hybridization for osteopontin, a possible marker of subset in activated microglia. Results : 1) In lesioned side of substantia nigra and corpus striatum, the TH immunoreactivity was markedly decreased in whole experimental groups. 2) Using optical densitometry, microglia induced immunoreactivity of OX-42 was counted at SN and corpus striatum. At SN, it was increased significantly on the lesioned side in control and all time-dependent experimental groups. At striatum, it was increased significantly in post lesion 3-day group only(p <0.05). Compared to control group, immunoreactivity of OX-42 on lesioned side was increased in groups, except post lesion 21-day group, at SN. Only post lesion 3-day group showed significance at striatum(p <0.05). Compared to SN region, immunoreactivity of OX-42 was much weaker in striatum. 3) Microscopically, the microglias showed typically different activation pattern. At SN, numerous phagocytic microglias were found at pars compacta and reticularis of lesion side. At striatum, no phagocytic form was found and the intensity of staining was much weaker. 4) At SN, the immunoreactivity of osteopontin showed definite laterality and it was markedly increased at pars compacta of lesion side with relatively short duration time. At striatum, however, it was not detected by in situ hybridization technique. Conclusion : The nigral 6-OHDA induced rat model of Parkinson's disease revealed several characteristic patterns of microglial reaction. At SN, microglias was activated shortly after direct neuronal damage and maintained for about three weeks. In contrast, despite of sufficient dopaminergic insufficiency at striatum, activation of microglias was trivial, and distinguished 3 day later. Antegrade slow neuronal degeneration is major pathophysiology in striatal dopaminergic deficiency. So, the acuteness of neuronal damage and consequential degree of neuronal degeneration may be important factor for microglial activation in neurodegenerative diseases such as Parkinson's disease. Additionally, osteopontin may be a possible marker for several subsets of activated microglia, possibly the phagocytic form.

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Antimicrobial Peptide, Lumbricusin, Ameliorates Motor Dysfunction and Dopaminergic Neurodegeneration in a Mouse Model of Parkinson's Disease

  • Kim, Dae Hong;Lee, Ik Hwan;Nam, Seung Taek;Hong, Ji;Zhang, Peng;Lu, Li Fang;Hwang, Jae Sam;Park, Ki Cheol;Kim, Ho
    • Journal of Microbiology and Biotechnology
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    • v.25 no.10
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    • pp.1640-1647
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    • 2015
  • We recently reported that the antimicrobial peptide Lumbricusin (NH2-RNRRWCIDQQA), isolated from the earthworm, increases cell proliferation in neuroblastoma SH-SY5Y cells. Here, we investigated whether Lumbricusin has neurotropic activity in mouse neural stem cells (MNSCs) and a protective effect in a mouse model of Parkinson's disease (PD). In MNSCs isolated from mouse brains, Lumbricusin treatment significantly increased cell proliferation (up to 12%) and reduced the protein expression of p27Kip1 through proteasomal protein degradation but not transcriptional regulation. Lumbricusin inhibited the 6-OHDA-induced apoptosis of MNSCs, and also showed neuroprotective effects in a mouse PD model, ameliorating the motor impairments seen in the pole, elevated body swing, and rotation tests. These results suggest that the Lumbricusin-induced promotion of neural cell proliferation via p27Kip1 degradation has a protective effect in an experimental PD model. Thus, the antimicrobial peptide Lumbricusin could possibly be developed as a potential therapeutic agent for the treatment of PD.

The Effect of Swimming and Minocycline on Motor Function and Expression of Bcl-2 after Spinal Cord Injury in the Rats (미노싸이클린과 수영훈련이 척수손상 흰쥐의 운동기능 및 Bcl-2발현에 미치는 영향)

  • Ha, Mi-Sook;Ha, Bae-Jin
    • Journal of Life Science
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    • v.19 no.10
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    • pp.1489-1494
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    • 2009
  • This study was designed to investigate the effects of swimming and minocycline on motor function recovery and Bcl-2 expression after spinal cord injury (SCI) in rats. After operation, neurological motor behavior test (BBB scale) on days 1, 4, 7, 10, and 14 were tested. Western blot and immunohistochemical assessment (Bcl-2) were performed on day 14. BBB scale started to show a statistically significant difference on day 7 (p<0.05). On day 14, it showed the most significant (p<0.05) difference. Expression of Bcl-2 increased in all the experimental groups. In particular, the highest expression of Bcl-2 appeared in the swimming and minocycline groups. Based on these results, minocycline and swimming were the most effective factors in the motor behavior function and immunohistochemical assessment of SCI rats.

The Antimicrobial Peptide CopA3 Inhibits Clostridium difficile Toxin A-Induced Viability Loss and Apoptosis in Neural Cells

  • Yoon, I Na;Hwang, Jae Sam;Lee, Joon Ha;Kim, Ho
    • Journal of Microbiology and Biotechnology
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    • v.29 no.1
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    • pp.30-36
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    • 2019
  • Numerous studies have reported that enteric neurons involved in controlling neurotransmitter secretion and motility in the gut critically contribute to the progression of gut inflammation. Clostridium difficile toxins, which cause severe colonic inflammation, are also known to affect enteric neurons. Our previous study showed that C. difficile toxin A directly induces neural cell toxicities, such as viability loss and apoptosis. In the current study, we attempted to identify a potent inhibitor of toxin A-induced neural cell toxicity that may aid in managing toxin A-induced gut inflammation. In our recent study, we found that the Korea dung beetle-derived antimicrobial peptide CopA3 completely blocked neural cell apoptosis caused by okadaic acid or 6-OHDA. Here, we examined whether the antimicrobial peptide CopA3 inhibited toxin A-induced neural cell damage. In neuroblastoma SH-SY5Y cells, CopA3 treatment protected against both apoptosis and viability loss caused by toxin A. CopA3 also completely inhibited activation of the pro-apoptotic factor, caspase-3. Additionally, CopA3 rescued toxin A-induced downregulation of neural cell proliferation. However, CopA3 had no effect on signaling through ROS/p38 $MAPK/p27^{kip1}$, suggesting that CopA3 inhibits toxin A-induced neural cell toxicity independent of this well-characterized toxin A pathway. Our data further suggest that ability of CopA3 to rescue toxin A-induced neural cell damage may also ameliorate the gut inflammation caused by toxin A.