• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1995년도 춘계학술대회
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• pp.101-101
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• 1995

The effects of ginseng prepation, Adaptagen$\^$R/ (AD), on the central dopaminergic nervous system in the learning-impaired rats were studied. The learning impaired rats were rendered by the intracerebroventricular infusion of ethylcholine aziridium (AF64A), 3 nmol/each side. Three days after the infusion of AF64A, AD were orally intubated daily for five days, 200 mg/kg. The control groups were intubated with distilled water. Twenty four hours after the last intubation, The changes in the specific bindings of dopamine receptors, the concentrations of dopamine (DA) and metabolites, The activities of tyrosine hydrosylase (TH) and monoamine oxidase (MAO) were analyzed using receptor radiography, HPLC-ECD and the methods in enzyme-assays, respectively.

• 한국동물학회지
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• 제38권2호
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• pp.238-247
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• 1995

쥐 뇌에·처 카드뮴에 대한 metallothionein-like protein(MTLP)의 유도 생성 능력을 알아보기 위하여 Stereotaxic Bpparatus를 이용하여 측뇌실에 카드뮴을 주사하여 다음과 같은 결과를 얻었다. 대조군과 생리식염수 처리군에서는 MTLP의 양적 변화가 없었고. 카드를 처리군은 대조군과 식염수 처리군에 비하여 MTLP가 2배 이상 유도되었다. MTLP의 분자량은 6.000-6,500 Oa 정도 였으며. 흡광도가 254 nm에서 높게 나타나고. 280 nm에서 낮게 나타나는 것으로 보아 thiol 함량이 높고 방향족 아미노산이 적은 단백질임을 알 수 있었다 또한 카드뮴 처리군에서는 MTLP 이외의 여러 종류의 protein-30. 64, 68, 80, 108 kDa-들이 유도되었다 이와 같은 결과로 카드뮴은 흰쥐 뇌에서도 MTLP의 유도 능력이 있음을 알 수 있었다.

• Archives of Pharmacal Research
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• 제26권5호
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• pp.411-415
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• 2003

To investigate the mechanisms involved in hemin-induced febrile response, the rectal temperature of rats were measured after intracerebroventricular (i.c.v.) injections of hemin, with or without antagonists. Hemin ($10\mu\textrm{g}$) elicited a significant febrile response, which lasted from 30 min, to more than 6 h, after its administration, but this was not the case with biliverdin (i.c.v.) and bilirubin (i.c.v.). The hemin-induced febrile response was significantly inhibited by pretreatment with an inhibitor of tyrosine kinase (genistein), but not by pretreatment with an inhibitor of protein kinase C (chelerythrine) and a scavenger of iron (deferoxamine). These results suggest that tyrosine kinase is involved in the hemin-induced febrile response.

• 대한약리학회지
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• 제23권2호
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• pp.87-94
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• 1987

스트레스로 인한 위궤양형성에 중추성 교감신경의 영향여부를 추구하기 위하여 norepinephrine, epinephrine, dopamine, isoproterenol 및 clonidine을 흰쥐의 뇌실내로 투여 하고 한냉 환경 $(4^{\circ}C)$에서 4시간 구속방치하여 위 분비기능의 변동과 궤양 발생 정도를 검색하여 다음과 같은 결과를 얻었다. 1. Norepinephrine, epinephrine, dopamine및 소량의 clonidine 처치로 궤양 발생이 현저하게 감소하였다. 2. Norepinephrine또는 epinephrine 처치군에서는 위액분비, 산분비 및 펩신 분비의 감소와 궤양 발생 감소가 초래되었다. 3. Dopamine혹은 소량의 clonidine 처치군에서는 궤양 발생의 감소와 위액분비 및 산분비 감소가 초래되었으나 펩신 분비는 변동 없었다. 4. Isoproterenol처치군에서는 궤양 발생과 펩신 분비는 대조군과 차이 없고, 위액분비 및 산분비의 감소만 나타났다. 5. 대량의 clonidine 투여군에서는 궤양발생, 산분비 및 펩신분비 모두 변동없이 약간의 위액분비 감소가 나타났다 이상의 결과로 보아 중추성 교감신경자극은 궤양 형성을 억압하는 작용이 있고, 이에는 교감신경성 ${\alpha}$-수용체 및 도파민성 수용체가 관여된다고 믿어지며, 이 효과는 위액분비 감소 및 산 분비 감소작용과 아울러 또 다른 요인이 관여한다고 추측된다.

• 대한약리학회지
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• 제29권1호
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• pp.23-32
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• 1993

GABA계가 뇌내의 교감신경계기능에 영향을 주어서 혈압조절에 관여함이 알려져 있다. 본 연구에서는 마취가토에서 GABA계가 두개내압증가에 의한 혈압상승에 관여하는가를 조사하였다. 두개내압증가에 의한 승압은 측뇌실내 muscimol (GABA 작용약)이나 clonidine $({\alpha}_2$-작용약) 전처리후에는 볼 수 없었다. 측뇌실내 yohimbine $({\alpha}_2$-길항약)으로 일으킨 고혈압은 두개내압증가를 하여도 더 이상 상승하지 않았으나, 측뇌실내 bicuculline (GABA 길항약)으로 일으킨 고혈압은 두개내압증가로 더욱 상승하였다. Bicuculline은 muscimol이나 clonidine 저혈압에서는 승압을 일으켰으나 yohimbine이나 두개내압증가에 의한 고혈압에서는 무효였다. Yohimbine은 clonidine 저혈압은 상승시켰으나 muscimol 저혈압에 있어서는 무효였다. Yohimbine은 두개내압증가에 따른 승압상태는 더 올리지 못하였으나 bicuculline 승압상태는 더욱 상승시켰다. Muscimol은 bicuculline과의 길항성이외에 yohimbine 승압을 억제함을 알았으며 yohimbine 승압에 GABA계가 관여함을 추측할 수 있었다. 이러한 실험결과로 두개내압증가에 따른 승압상승은 (1) ${\alpha}_{2}$-수용체, (2) bicuculline-감수성 GABA 수용체, (3) yohimbine-감수성인 clonidine이 작용하는 GABA계 부위의 세가지 방법으로 억제성인 교감신경기능을 불활성화하여 일어나는 것으로 추론하였다.

• 대한본초학회지
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• 제28권1호
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• pp.83-90
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• 2013

Objectives : Tetramethylpyrazine (TMP) is an active ingredient in Ligusticum wallichii and has a wide range of neuroprotection effects. This study investigated anti-neuroinflammatory effect of TMP on brain regions in intracerebroventricular (i.c.v.) lipopolysaccharide (LPS)-treated C57BL/6 mice. Methods : TMP was administered intraperitoneally at doses of 10, 20, and 30 mg/kg at 1 h prior to LPS (3 mg/kg) i.c.v. injection. mRNA level of pro-inflammatory cytokines, including tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin (IL)-$1{\beta}$ and IL-6, was measured in the cerebral cortex, hippocampus, and hypothalamus tissue using real-time polymerase chain reaction at 24 h after the LPS injection. Cyclooxygenase-2 (COX-2) positive cells in the hypothalamus was also observed using immunohistochemistry at 24 h after the LPS injection. Results : At a dose of 30 mg/kg TMP significantly attenuated up-regulation of TNF-${\alpha}$ and IL-$1{\beta}$ mRNA in the cerebral cortex and IL-$1{\beta}$ mRNA in the hippocampus. In the hypothalamus, doses of 20 mg/kg and 30 mg/kg TMP significantly attenuated up-regulation of TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 mRNA induced by the LPS injection. In addition, TMP (30 mg/kg) significantly reduced the number of COX-2 positive cells in the hypothalamus. Conclusion : These results indicate that TMP has an anti-inflammatory effect on neuroinflammation, especially in the hypothalamus, induced by LPS i.c.v. injection and suggest that TMP-containing Ligusticum wallichii may play a modulatory role on the systemic responses following hypothalamic inflammation.

• Biomolecules & Therapeutics
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• 제23권3호
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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 $NF{\kappa}B$.

• Biomolecules & Therapeutics
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• 제17권4호
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• pp.362-369
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• 2009

We have investigated the effect of glucosamine on the retinal cells after continuous infusion into cerebroventricle by using osmotic minipump to avoid peripheral effect. Continuous intracerebroventricular (i.c.v) infusion of glucosamine with the rate of 0.1 ${\mu}mol$/10 ${\mu}l$/hr for 7 days resulted in morphological changes of the optic nerve in electron microscopic level as well as morphological changes of the retina in light microscopic level. Retinal sections were immunostained for the detection of morphological changes of astrocytes. GFAP immunoreactivity appeared not only in the Muller cells but also many of the radial processes of Muller cells. The optic nerve showed deformed axon and slight lamellar separation of myelin sheath after continuous infusion of glucosamine in observing with electron microscope. Interestingly, vacuoles were observed in deformed axons and retinal layers were folded and detached. These results suggested that glucosamine plays a role in induction of morphological dysfunction in retina and optic nerves.

• 대한약리학회지
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• 제16권2호
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• pp.1-7
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• 1980

As it has been reported that morphine induce antidiuresis, and antinatriuresis along with decrease in renal hemodynamics when given intracerebroventricularly[ivt], the renal action of nalorphine, a partial antagonist of morphine action, and its influence upon the morphine action were investigated in this study. $10{\mu}g/kg$ of nalorphine given into the lateral ventricle of the rabbit brain tended to decrease renal plasma flow and glomerular filtration rate and increase the reabsorption of free water in the tubules. $100{\mu}g/kg$ ivt significantly decreased urine flow rate and increased free water reabsorption, and tended to increase electrolyte excretion in spite of decrease in renal plasma flow and glomerular filtration, suggesting that ADH also involved in the antidiuresis. Morphine hydrochloride, $10{\mu}g/kg$, ivt, produced marked decrement in renal hemodynamics along with decreased excretions of sodium, potassium and water, and these morphine actions were alleviated by nalorphine given 20 min later. The natriuretic action of ivt nalorphine manifested itself uninfluenced by the morphine. These observations indicate that nalorphine ivt produces renal actions similar to those of morphine, though less potent, and that it can antagonize the latter action. It is suggested that morphine influences renal hemodynamics through nerve by stimulating the 'morphine receptor' in the brain, whereas nalorphine liberates ADH by the agonistic action on the 'nalorphine receptor'.

• Natural Product Sciences
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• 제26권3호
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• pp.221-229
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• 2020

This study was undertaken to investigate the protective effect of rice bran oil (RBO) on amyloid β protein (Aβ) (25-35)-induced memory impairment and brain damage in an ICR mouse model. Memory impairment was produced by intracerebroventricular microinjection of 15 nmol Aβ (25-35) and assessed using the passive avoidance test. Treatment with RBO at 0.1, 0.5, or 1 mL/kg (p.o. daily for 8 days) protected against Aβ (25-35)-induced memory impairment. Furthermore, Aβ (25-35)-induced decreases in glutathione and increases in lipid peroxidation and cholinesterase activity in brain tissue were inhibited by RBO, and Aβ (25-35)-induced increases of phosphorylated mitogen-activated protein kinases (MAPKs) and inflammatory factors, and changes in the levels of apoptosis-related proteins were significantly inhibited by RBO. Furthermore, Aβ (25-35) suppressed the PI3K/Akt pathway and the phosphorylation of CREB, but increased phosphorylation of tau (p-tau) in mice brain; these effects were significantly inhibited by administration of RBO. These results suggest that RBO inhibits Aβ (25-35)-induced memory impairment by inducing anti-apoptotic and anti-inflammatory effects, promoting PI3K/Akt/CREB signaling, and thus, inhibiting p-tau formation.