• Title/Summary/Keyword: model rat

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Effect of Ginseng on Fat Accumulation in the Obese Rats Induced by High Fat Diet (인삼이 고지방식이에 의한 비만유도 Rat에서 지방축적에 미치는 영향)

  • 김신일;김영숙
    • Journal of Ginseng Research
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    • v.10 no.2
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    • pp.167-179
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    • 1986
  • Obesity is common disease resultly accumulated excess fat. In the model for obesity induced by high fat diet contains 30% fat, administration of ginseng extract inhibited increment of body weight, epididymal fat pads and enlargement of fat cell size. This was as the result of inhibition of lipogenesis in the liver and fat accumulation in the adipose tissues.

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Development of Glioblastoma In Vivo Model for the Research of Brain Cancer Diagnosis and Therapy (뇌암 진단 및 치료 연구를 위한 교모세포종 동물모델 개발)

  • Kang, Seonghee;Kang, Bosun
    • Journal of the Korean Society of Radiology
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    • v.8 no.7
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    • pp.389-395
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    • 2014
  • The research was carried out to develop a animal model of malignant brain tumor for the researches in glioblastoma multiform (GBM) diagnosis and therapy. C6 cells were transplanted into the right striatum of SD rat using stereotactic instrument for the development. The developed animal model was verified by MRI and H&E stain assay of anatomicohistological examination. The MRI observations showed that the tumor developed at the injection site at the 7 days after glioblastoma inoculation. At 14 days post inoculation, the tumor grew to a large volume occupying almost a half of the right cerebral hemisphere. It was confirmed that the expression of excessive mitosis and pleomorphism in anatomicohistological examination. The developed animal model must be necessary and useful tool for the in vivo level research in the development of the new modality for the diagnosis and therapy of brain cancer.

Temporal Expression of Interleukin-1${\beta}$ in the Dorsal Root Ganglion in a Rat Model of Lumbar Disc Herniation

  • Kim, Su-Jeong;Gu, Hee-Jin;Cho, Yun-Woo;Park, Hea-Woon;Lee, Joon-Ha;Hwang, Se-Jin;Ahn, Sang-Ho
    • The Journal of Korean Physical Therapy
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    • v.22 no.3
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    • pp.93-98
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    • 2010
  • Purpose: To investigate temporal changes in IL-1${\beta}$ mRNA expression in spinal dorsal horn (DH) and dorsal root ganglion (DRG) in a rat lumbar disc herniation (LDH) model. Methods: Autologous nucleus pulposus, harvested from the tail disc between the second and third coccygeal vertebrae (Co2-3), was implanted next to the left L5 nerve root just proximal to the DRG after partial laminectomy. IL-1${\beta}$ mRNA expression was investigated in DRG and DH in our LDH model. Real-time PCR assays were done using a 7500 Real Time PCR system (Applied Biosystems, USA). Results: Expression of IL-1${\beta}$ in DRG and DH was observed for 30 days postoperatively. Expression of IL-1${\beta}$ mRNA in the ipsilateral DRG of the LDH group gradually increased from 5 to 30 days after surgery. The amount of IL-1${\beta}$ in the contralateral DRG peaked 10 days after surgery and then gradually decreased. However, there was no difference in IL-1${\beta}$ mRNA expression in spinal DH between the LDH group and the sham-operated group. Conclusion: Long-term expression of IL-1${\beta}$ in the LDH model may worsen the chronic pain state. Future studies on inhibition of IL-1${\beta}$ expression in the LDH model will be needed to develop selective treatment strategies for patients with LDH.

Olanzapine Attenuates Mechanical Allodynia in a Rat Model of Partial Sciatic Nerve Ligation

  • Fukuda, Taeko;Yamashita, Soichiro;Hisano, Setsuji;Tanaka, Makoto
    • The Korean Journal of Pain
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    • v.28 no.3
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    • pp.185-192
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    • 2015
  • Background: Neuropathic pain is a global clinical problem; nevertheless, nerve injury treatment methods remain limited. Olanzapine has antinociceptive and anti-nueropathic properties; however, its preventive effects have not been assessed in nerve injury models. Methods: We prepared a partial sciatic nerve ligation (Seltzer model) or sham-operated model in male Sprague-Dawley rats under isoflurane anesthesia. In a pre-treatment study, we administered olanzapine (10 mg/kg) intraperitoneally 1 h before nerve ligation. In post-treatment and dose-dependent studies, we injected 3 different doses of olanzapine intraperitoneally 1 h after nerve ligation. Mechanical allodynia was measured before and 7 days after surgery. Immunohistochemical analysis using anti-Iba-1 antibody was used to assess the effect of olanzapine at the spinal level. Results: In the pre-treatment study, median withdrawal thresholds of the normal saline groups were significantly lower than those of the sham-operated groups; however, those of the olanzapine (10 mg/kg) and sham-operated groups were not different. In the post-treatment and dose-dependent studies, the median withdrawal thresholds of the olanzapine (2.5 mg/kg) and normal saline groups were not different; however, those of the olanzapine (10 and 50 mg/kg) groups were significantly higher than those of the normal saline groups. Olanzapine did not have a significant effect on the density of Iba-1 staining. Conclusions: Olanzapine attenuated mechanical allodynia dose-dependently in the Seltzer model. This anti-allodynic effect of olanzapine was observed even when injected 1 h after nerve ligation. This effect of olanzapine appeared to be unrelated to microglia activation in the ipsilateral dorsal horn of the lumbar spinal cord.

Neuroprotective Effects of KC0244, a Glycine Site Antagonist, in a Rat Model of Transient Focal Ischemia

  • Ku, Hee-Jung;Churlmin Seong;Park, No-Sang;Changbae Jin
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 1998.11a
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    • pp.143-143
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    • 1998
  • Antagonists acting at the glycine site of the NMDA receptor have been gaining safer alternatives for stroke therapy because they have few adverse effect competitive and noncompetitive NMDA antagonists. Therefore, the neuroprotect novel glycine site antagonist KC0244 were evaluated in a rat model of transient comparison with GV150526A in a developmental phase. Middle cerebral artery oc was produced by insertion of a silicone-coated 4-0 nylon monofilament to the o in male Sprague-Dawley rats under isoflurane anesthesia. After 90 or 120 min retracted and the ischemic tissue reperfused. In 90-min MCAO model, GV150526A was administered 30 min before MCAO or immediately after MCAO. In 120-min MC KC0244 or GV150526A (10 mg/kg, i.p.) was administered 1 hr before MCAO or imme MCAO. Infarct volume was measured 24 hr after MCAO using the 2,3,5-triphe chloride staining method. In 90-min MCAO model, treatments with GV1505 significantly reduce infarct volume although they tended to slightly reduce cor approximately 19% compared with the nontreated group. In 120-min MCAO model with GV150526A did not either significantly reduce infarct volume although the reduce total infarct volume by approximately 16% compared with the vehicle-tre However, 1-hr preischemic and immediate treatments with KC0244 reduced total i 39 and 30% (corrected total infarct volume by 44 and 32%), respectively, co vehicle-treated control group. The results suggest that KC0244 can provid against transient focal ischemic damage with greater in vivo potency than GV150

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Cerebral Oxygenation Monitoring during a Variation of Isoflurane Concentration in a Minimally Invasive Rat Model

  • Choi, Dong-Hyuk;Kim, Sungchul;Shin, Teo Jeon;Kim, Seonghyun;Kim, Jae Gwan
    • Current Optics and Photonics
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    • v.6 no.5
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    • pp.489-496
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    • 2022
  • Our previous study on monitoring cerebral oxygenation with a variation of isoflurane concentration in a rat model showed that near-infrared spectroscopy (NIRS) signals have potential as a new depth of anesthesia (DOA) index. However, that study obtained results from the brain in a completely invasive way, which is inappropriate for clinical application. Therefore, in this follow-up study, it was investigated whether the NIRS signals measured in a minimally invasive model including the skull and cerebrospinal fluid layer (CSFL) are similar to the previous study used as a gold standard. The experimental method was the same as the previous study, and only the subject model was different. We continuously collected NIRS signals before, during, and after isoflurane anesthesia. The isoflurane concentration started at 2.5% (v/v) and decreased to 1.0% by 0.5% every 5 min. The results showed a positive linear correlation between isoflurane concentration and ratio of reflectance intensity (RRI) increase, which is based on NIRS signals. This indicates that the quality of NIRS signals passed through the skull and CSFL in the minimally invasive model is as good as the signal obtained directly from the brain. Therefore, we believe that the results of this study can be easily applied to clinics as a potential indicator to monitor DOA.

Anti-inflammatory Effects of Co-treatment of Jingyoganghwaltang and Cheongsimhwan on Croton Oil Induced Hemorrhoid Model in Rats

  • Jo, Nayoung;Mou, Jong-Cheng;Leem, Kanghyun;Kim, Taeyeon
    • The Korea Journal of Herbology
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    • v.33 no.6
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    • pp.79-86
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    • 2018
  • Objectives : Hemorrhoids are one of the most common diseases in humans. Jingyoganghwaltang (JG) and Cheongsimhwan (CS) have been used for treating hemorrhoids in Korean traditional clinical practice. The present study was designed to evaluate the traditional effects of JG and CS on the experimental hemorrhoid model in rats. Methods : Hemorrhoids are closely related to inflammation. Accordingly, we examined the nitric oxide (NO) production in macrophage cell line in order to evaluate the anti-inflammatory effect. The expression levels of inflammation related genes including IL-1 beta, IL-6, INOS, and TNF-alpha were examined via a real-time quantitative PCR. Croton oil-induced hemorrhagic animal model was used to test the in vivo efficacy against hemorrhoids. The rectal tissues were weighed and the inflammatory proteins were measured to confirm the anti-inflammatory effects. Results : JG and CS have a statistically significant effect on inhibition of NO production and on the reduction of inflammatory gene expression such as IL-1 beta, IL-6, INOS, and TNF-alpha. The synergistic effects of co-treatment of JG and CS were found out in the IL-6 gene expression. The in vivo study using croton oil-induced hemorrhoid model in rat was performed to check the co-treatment effects. As a result, the co-treatment reduced the inflammation of the rectal tissue and decrease the inflammation related protein productions including ICAM1, MMP2 and MMP9. Conclusions : These results suggest that JG and CS co-treatment demonstrated anti-inflammatory effects in croton oil-induced hemorrhoid model in rat.

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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