• Proceedings of the Korean Society of Applied Pharmacology
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• 1995.04a
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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.

• The Korean Journal of Zoology
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• v.38 no.2
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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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• v.26 no.5
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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.

• The Korean Journal of Pharmacology
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• v.23 no.2
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• pp.87-94
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• 1987

The role of central adrenergic activity in the genesis of stress ulcers was investigated by intracerebroventricular (i.c.v.) administration of catecholamines and clonidine in pylorus-ligated rats restrained for 4 hours at a temperature of $4^{\circ}C$. 1. The stress-induced ulceration was markedly decreased by the i.c.v. administration of norepinephrine, epinephrine, dopamine or low dose of clonidine. 2. After an i.c.v. administration of norepinephrine or epinephrine, the volume of gastric juice, and both acid and pepsin secretion were markedly decreased. 3. Dopamine or a low dose of clonidne decreased the volume of gastric juice and acid secretion but did not affect pepsin secretion. 4. Isoproterenol caused a decrease in the volume of gastric juice and acid secretion, however, the ulcerogenesis was similar to that of the control. 5. Gastric function as well as ulcerogenesis was little affected by a high dose of clonidine. From the above results, it is suggested that central adrenergic activation inhibits cold-restraint induced ulcerogenesis via adrenergic alpha and dopaminergic receptors, and that this effect may be mediated by a decrease in gastric acid secretion. It is also suggested that other factors may be involved in this antiulcerogenic effect.

• The Korean Journal of Pharmacology
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• v.29 no.1
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• pp.23-32
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• 1993

Recent studies have shown that a GABAergic mechanism in the brain modulates arterial blood pressure (BP) through alterations of sympathetic activity in the brain. The purpose of the present study was to determine if this modulation is involved in the pressor response to raised intracranial pressure (ICP). The pressor response to raised ICP was abolished by pretreatment of anesthetized rabbits with intracerebroventricular (icv) muscimol (a GABA agonist) as well as with icv clonidine $(an\;{\alpha}_2-agonist)$. Raising ICP in the hypertensive state after icv yohimbine $(an\;{\alpha}_2-antagonist)$ did not cause an additional increase in the BP, whereas raising ICP in the hypertensive state following icv bicuculline (a GABA antagonist) produced a further increase. Bicuculline produced an increase of the BP which had been lowered by muscimol or by clonidine, whereas it failed to increase the hypertensive state induced by either previous yohimbine or raised ICP. Yohimbine reversed the BP which had been made low by clonidine but was incapable of raising the hypotensive state after muscimol. Yohimbine failed to increase the heightened BP due to raised ICP, whereas bicuculline-induced pressor state was further elevated by yohimbine. Muscimol, besides the bicuculline-antagonizing property, inhibited the pressor response to yohimbine, suggesting participation of a GABAergic mechanism in the pressor action of yohimbine. From these results it was inferred that there were three ways in which BP could be increased via raised ICP: inactivation of the inhibitory sympathetic activity through (1) ${\alpha}_{2}-adrenoceptors$, (2) bicuculline-sensitive GABA receptors, (3) yohimbine-sensitive, clonidine-acting GABAergic sites.

• The Korea Journal of Herbology
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• v.28 no.1
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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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• 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 $NF{\kappa}B$.

• Biomolecules & Therapeutics
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• v.17 no.4
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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.

• The Korean Journal of Pharmacology
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• v.16 no.2 s.27
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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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• v.26 no.3
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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.