• Title/Summary/Keyword: Mouse Brain

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Comparative study on Hsp25 expression in Mongolian gerbil and mouse cerebellum

  • Lee, Heang-Yeon;Kim, Seong-Hwan;Lee, Jae-Bong;Shin, Chang-Ho
    • Korean Journal of Veterinary Service
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    • v.29 no.4
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    • pp.469-482
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    • 2006
  • The term 'heat shock protein (Hsps)' was derived from the fact that these proteins were initially discovered to be induced by hyperthermic conditions. In response to a range of stressful stimuli, including hyperthermia, immobilization, UV radiation, amino acid analogues, arsenite, various chemicals, and drugs the mammalian brain demonstrates a rapid and intense induction of the heat shock protein. Moreover, Hsps were expressed on the various pathological conditions including trauma, focal or global ischemia, hypoxia, infarction, infections, starvation, and anoxia. Especially, Hsp25 has a protective activity, facilitated by the ability of the protein to decrease the intracellular levels of reactive oxygen species (ROS) as well as its chaperone activity, which favors the degradation of oxidized proteins. Recently, it has clearly demonstrated that Hsp25 is constitutively expressed in the adult mouse cerebellum by parasagittal bands of purkinje cells in three distinct regions, the central zone (lobule VI-VII) and nodular zone (lobule IX-X), and paraflocculus. The Mongolian gerbil has been introduced into stroke study model because of its unique brain vasculature. There are no significant connections between the basilarvertebral system and the carotid system. This anatomy feature renders the mongolian gerbil susceptible to forebrain ischemia-induced seizure. The present study is designed to examine the pattern of Hsp25 expression in the cerebellum of this animal in comparison with that in mouse.

Effect of Antioxidant Enzymes on Hypoxia-Induced HIF-$1{\alpha}$ Accumulation and Erythropoietin Activity

  • Cho, Eun-Jin;Cho, Ki-Woon;Chung, Kyoung-Jin;Yang, Hee-Young;Park, Hyang-Rim;Park, Byung-Ju;Lee, Tae-Hoon
    • International Journal of Oral Biology
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    • v.34 no.4
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    • pp.205-213
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    • 2009
  • The mechanisms underlying the actions of the antioxidants upon reactive oxygen species (ROS) generation by NADPH oxidase complex have remained uncertain. In this study, we investigated NADPH oxidase activity and the role of antioxidant enzymes upon the generation of ROS during hypoxic stress. ROS generation was found to increase in the mouse kidney under hypoxic stress in a time-dependent manner. Moreover, we found in MCT cells that hypoxia-induced hydrogen peroxide production was decreased by NAC pretreatment. We further analyzed HIF-$1{\alpha}$, PHD2 and VHL expression in the NAC-pretreated MCT cells and assessed the response of antioxidant enzymes at the transcriptional and translational levels. SOD3 and Prdx2 were significantly increased during hypoxia in the mouse kidney. We also confirmed in hypoxic $Prdx2^{-/-}$ and SOD3 transgenic mice that erythropoietin (EPO) is transcriptionally regulated by HIF-$1{\alpha}$. In addition, although EPO protein was found to be expressed in a HIF-$1{\alpha}$ independent manner in three mouse lines, its activity differed markedly between normal and $Prdx2^{-/-}$/SOD3 transgenic mice during hypoxic stress. In conclusion, our current results indicate that NADPH oxidase-mediated ROS generation is associated with hypoxic stress in the mouse kidney and that SOD3 and Prdx2 cooperate to regulate cellular redox reactions during hypoxia.

Regulation of Apoptosis and Cell Cycle in Irradiated Mouse Brain (마우스의 대뇌조직에서 방사선에 의한 아포토시스와 세포주기의 조절)

  • Oh, Won-Yong;Song, Mi-Hee;Chung, Eun-Ji;Seong, Jin-Sil;Suh, Chang-Ok
    • Radiation Oncology Journal
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    • v.19 no.2
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    • pp.146-152
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    • 2001
  • Purpose : To investigate the regulation of apoptosis and cell cycle in mouse brain irradiation. Materials and Methods : 8-week old male mice, C57B1/6J were given whole body $\gamma-radiation$ with a single dose of 25 Gy using Cobalt 60 irradiator. At different times 1, 2, 4, 8 and 24hr after irradiation, mice were killed and brain tissues were collected. Apoptotic cells were scored by TUNEL assay. Expression of p53, Bcl-2, and Bax and cell cycle regulating molecules; cyclins Bl, Dl, E and cdk2, cdk4, $p34^{cdc2}$ were analysed by Western blotting. Cell cycle was analysed by Flow cytometry. Results : The peak of radiation induced apoptosis is shown at 8 hour after radiation. With a single 25 Gy irradiation, the peak of apoptotic index in C57B1/6J is $24.0{\pm}0.25$ (p<0.05) at 8 hour after radiation. Radiation upregulated the expression of p53/tubulin, Bax/tubulin, and Bcl-2/tubulin with 1.3, 1.1 and 1.45 fold increase, respectively were shown at the peak level at 8 hour after radiation. The levels of cell cycle regulating molecules after radiation are not changed significantly except cyclin D1 with 1.3 fold increase. Fractions of Go-Gl, G2-M and S phase in the cell cycle does not specific changes by time. Conclusion : In mouse brain tissue, radiation induced apoptosis is particularly shown in a specific area, subependyma. These results and lack of radiation induced changes in cell cycle ofter better understanding of radiation response of noraml brain tissue.

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Effect of Pioglitazone on Excitotoxic Neuronal Damage in the Mouse Hippocampus

  • Lee, Choong Hyun;Yi, Min-Hee;Chae, Dong Jin;Zhang, Enji;Oh, Sang-Ha;Kim, Dong Woon
    • Biomolecules & Therapeutics
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    • v.23 no.3
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    • pp.261-267
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    • 2015
  • Pioglitazone (PGZ), a synthetic peroxisome proliferator-activated receptor ${\gamma}$ agonist, is known to regulate inflammatory process and to have neuroprotective effects against neurological disorders. In the present study, we examined the effects of 30 mg/kg PGZ on excitotoxic neuronal damage and glial activation in the mouse hippocampus following intracerebroventricular injection of kainic acid (KA). PGZ treatment significantly reduced seizure-like behavior. PGZ had the neuroprotective effect against KA-induced neuronal damage and attenuated the activations of astrocytes and microglia in the hippocampal CA3 region. In addition, MPO and $NF{\kappa}B$ immunoreactivities in the glial cells were also decreased in the PGZ-treated group. These results indicate that PGZ had anticonvulsant and neuroprotective effects against KA-induced excitotocix injury, and that neuroprotective effect of PGZ might be due to the attenuation of KA-induced activation in astrocytes and microglia as well as KA-induced increases in MPO and $NF{\kappa}B$.

Diversification of the molecular clockwork for tissue-specific function: insight from a novel Drosophila Clock mutant homologous to a mouse Clock allele

  • Cho, Eunjoo;Lee, Euna;Kim, Eun Young
    • BMB Reports
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    • v.49 no.11
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    • pp.587-589
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    • 2016
  • The circadian clock system enables organisms to anticipate the rhythmic environmental changes and to manifest behavior and physiology at advantageous times of the day. Transcriptional/translational feedback loop (TTFL) is the basic feature of the eukaryotic circadian clock and is based on the rhythmic association of circadian transcriptional activator and repressor. In Drosophila, repression of dCLOCK/CYCLE (dCLK/CYC) mediated transcription by PERIOD (PER) is critical for inducing circadian rhythms of gene expression. Pacemaker neurons in the brain control specific circadian behaviors upon environmental timing cues such as light and temperature cycle. We show that amino acids 657-707 of dCLK are important for the transcriptional activation and the association with PER both in vitro and in vivo. Flies expressing dCLK lacking AA657-707 in $Clk^{out}$ genetic background, homologous to the mouse Clock allele where exon 19 region is deleted, display pacemaker-neuron-dependent perturbation of the molecular clockwork. The molecular rhythms in light-cycle-sensitive pacemaker neurons such as ventral lateral neurons ($LN_vs$) were significantly disrupted, but those in temperature-cycle-sensitive pacemaker neurons such as dorsal neurons (DNs) were robust. Our results suggest that the dCLK-controlled TTFL diversify in a pacemaker-neuron-dependent manner which may contribute to specific functions such as different sensitivities to entraining cues.

The Antioxidant Effects of Sesimting on the Brain Tissue of Rat (세심탕(洗心湯)이 뇌조직(腦組織)의 산화작용(酸化作用)에 미치는 영향(影響))

  • Kim Seong-Hyeon;Lee Sang-Ryong
    • Journal of Oriental Neuropsychiatry
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    • v.8 no.2
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    • pp.39-50
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    • 1997
  • This experiment was to investigate the antioxidant effect of Sesimtang(SST) on brain tissues of mouse. The experimental groups were divided into three groups and treated ad follows for 15 days ; Normal group(NC), Vt.E admistrated group(PC), SST administrated Group(SST). After the extracting microsome from brain of mouse, those were measured the amounts of oxidant materials like MDA(malonaldehyde) and $H_2O_2$, then activities of antioxidant enzymes like SOD(superoxide dismutase), catalase, NADPH-cytochrome P-450 reductase. The results were as follows; 1. In TBA reaction to measure the amount of MDA, oxidant material of brain tissue of aged rat, both treated groups showed significant decrease. 2. Hydrogen peroxide formation was showed significant decrease in both treated groups than normal group. 3. Superoxide dismutase activity was increased in both treated groups than normal group, and showed little change in SST administrated group than normal group. 4. Catalase activity was increased in both treated groups than normal group. 5. NADPH-cytochrome P-450 reductase activity was increased in both treated groups than normal group.

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Cadmium Altered Gene Expression Related to Zinc Homeostasis in the Mouse Brain (카드뮴이 마우스 뇌에서 아연의 항상성에 관여하는 유전자발현에 미치는 영향)

  • Park Jong-An;Yoe Eun-Young;Nam Sang-Hun;Jang Bong-Ki;Lee Jong-Wha;Kim Wan-Jong
    • Environmental Analysis Health and Toxicology
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    • v.19 no.4
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    • pp.389-399
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    • 2004
  • Metallothionein (MT), a small protein molecule which can bind or release metal ions, is involved in the regulation of cellular metal homeostasis. This study was investigated the accumulation of cadmium in blood, tissue (liver, kidney and brain), and the effect of cadmium on several key genes (MT-I, MT-II, ZnT-1) in zinc metabolism in the mouse. Mouses weighing 20∼25 g were randomly assigned to control and cadmium treated group (Cd group). Cd group was intraperitoneally injected with cadmium 2, 4, 8 mg/kg and control group was administerd with saline. Mouses of each group were sacrificed by decapitation 4 hours after the administration of cadmium. Cadmium contents in blood, liver, kidney and brain were increased by a dose-dependent manner. Accumulation of cadmium was mainly occurred in liver and kidney. Induction of MT-I and MT-II protein was increased, but ZnT-1 expression was decreased in a dose-dependent manner by the treatment of 2∼8 mg/kg cadmium. These results suggested that cadmium can be transported to brain and alter the expression of several key genes in zinc homeostasis.

The Efficacy of 9-($\beta$-D-Arabinofuranosyl)adenine and its Conjugate of Prednisone (BR-8702-AP) in the Treatment of Herpes simplex Virus Type 1 Encephalitis in Mice (단순 포진 바이러스 감염 생쥐에 대한 아데닌 아라비노사이드와 그의 프레드니손 결합화합물인 BR-8702-AP의 항바이러스 효과)

  • 채희상;신원섭;신현종;백우현
    • Biomolecules & Therapeutics
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    • v.1 no.1
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    • pp.98-102
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    • 1993
  • The therapeutic effectiveness of adenine arabinoside(tora-A) and its conjugate of prednisone(BR-8702-AP) was compared in Herpes simplex Virus Type 1 (HSV-1) infected BALB/C mice. The BALB/C mouse was infected with HSV-1(700 PFU/mouse) intranasally. Among mice infected intranasally with virus, a mortality rate of 100% was observed. On the oral administration of non-toxic doses of ara-A or BR-8702-AP(125 mg /kg/day) for 5 consecutive days 2 hours after virus infection, the tora-A was highly effective in reducing mortality to 0% (P<0.001) and BR-8702-AP was also effective in reducing mortality to 15% (P<0.01). In this model infection, the virus was first replicated in the lung and transmitted to the brain. Both arts-A and BR-8702-AP did not inhibit the viral replication in the lung, but they inhibited the viral transmission to the brain. However, the BR-8702-AP was less effective than the aria-A to prevent transmission of virus to brain. Therefore, the reduced mortality due to tora-A or BR-8702-AP therapy was associated with inhibition of viral transmission to brain.

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Oral Administration of Bifidobacterium lactis Ameliorates Cognitive Deficits in Mice Intracerebroventricularly Administered Amyloid Beta via Regulation the Activation of Mitogen-activated Protein Kinases

  • Jong Kyu Choi;Oh Yun Kwon;Seung Ho Lee
    • Food Science of Animal Resources
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    • v.44 no.3
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    • pp.607-619
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    • 2024
  • Probiotics are functional microorganisms that exhibit various biological activities, such as allergic reactions, inflammation, and aging. The aim of this study is to evaluate the effects of Bifidobacterium lactis CBT BL3 (BL) on the amyloid beta (Aβ)-mediated cognitive impairments. Oral administration of live BL to intracerebroventricularly Aβ-injected mice significantly attenuated short- and long-term memory loss estimated using the Y-maze and Morris water maze tests. We found that expression of apoptosisrelated proteins such as caspase-9, caspase-3, and cleaved poly (ADP-ribose) polymerase was significantly elevated in the brain tissues of Aβ-injected mouse brains when compared to that of the control mouse group. Interestingly, these expression levels were significantly decreased in the brain tissue of mice fed BL for 6 wk. In addition, the abnormal over-phosphorylation of mitogen-activated protein kinases (MAPKs) such as ERK1/2, p38 MAPK, and JNK in the brain tissue of intracerebroventricularly Aβ-injected mice was significantly attenuated by oral administration of BL. Taken together, the results indicate that Aβ-induced cognitive impairment may be ameliorated by the oral administration of BL by controlling the activation of MAPKs/apoptosis in the brain. This study strongly suggests that BL can be developed as a functional probiotic to attenuate Aβ-mediated cognitive deficits.

Mouse Somatosensory Cortex Stimulation Using Pulse Modulated Transcranial Magnetic Stimulation (구형파 변조된 경두개 자기자극을 이용한 쥐의 감각피질 자극실험)

  • Sun, Sukkyu;Seo, Taeyoon;Huh, Yeowool;Cho, Jeiwon;Kwon, Youngwoo
    • The Journal of Korean Institute of Electromagnetic Engineering and Science
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    • v.27 no.5
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    • pp.482-485
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    • 2016
  • In this work, a transcranial magnetic stimulation(TMS) experiment on animals is performed to stimulate the brain cortex of the mouse using modulated signals. The proposed TMS system is composed of the inverter, transformer, capacitor, variable inductor, and stimulation coil to generate 1.5 mT magnetic field in the brain cortex of the mouse. The stimulation signal is modulated to square wave where the carrier frequency is swept from 85 to 91 kHz to investigate the stimulation effect. The experimental result shows that when the carrier frequency of the stimulation signal is lower than 89 kHz, the reaction of the mouse does not change while the stimulation signal which has the carrier frequency higher than 89 kHz results in decreasing the threshold of the stimulus for the pressure.