• 혜화의학회지
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• 제18권2호
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• pp.1-12
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• 2009

Most of the cholesterol is synthesized by liver in the body while about one of third is taken via dietary. The main functions of cholesterol is to protect membranes in cell surface, avoid the arterial bleeding by hypertension, and prolong the life of erythrocytes, and so on. However, overload of cholesterol leads to arteriosclerosis associated with leading death cause. Lack of physical activity, emotional and environmental stress, and low intake of protein or vitamin E induce the unbalance between HDL- and LDL-cholesterol so become a basis of ischemic disorders in heart, brain and elsewhere in the body. So far, four major classes of medications for hyperlipidemia are HMG-CoA reductase inhibitors (statins), bile acid sequestrants, nicotinic acid, and fibric acids. The statins can lower LDL and levels triglyceride, but may induce myopathy and an elevation of liver enzyme levels. The bile acid sequestrants lower LDL levels and raise HDL levels with no effect on triglyceride levels but side effects of gastrointestinal (GI) distress, constipation, and a decrease in the absorption of other drugs. Nicotinic acid and fibric acids lower LDL and triglyceride levels with showing flushing, hyperglycemia, hyperuricemia, GI distress, and hepatotoxicity dyspepsia, gallstones, myopathy, and unexplained noncardiac death as adverse effects. Above western drugs lower cholesterol by 15 to 30% while all have notable adverse effects. In traditional medicine, hyperlipidemia is regarded as retention of phlegm and fluid disease. Etiology and pathogenesis of hyperlipidemia is basically based on Spleen-Deficiency and Phlegm-Stagnation, accumulation and stasis of -heat, and Qi & blood stagnation induced by Phlegm-damp, water-dampness, and blood stasis. Thereby, strengthening Spleen and dissolving Phlegm, clearing away heat and diuresis, and supplementing Qi and activating blood circulation are commonly used therapeutic methods for hyperlipidemia. The traditional herbal medicine, have been used for patients with CVA, hypertension or hyperlipidemia in Oriental hospital or Oriental clinic. The lock and key theory is used to develop most of western medicine, however many diseases are caused by mixed factors in body-complex system. We expect that Oriental pharmacological theory could be newborn as a novel drug showing high advantage of blood levels of lipidsand QOL of performance without side effects.

• 한국식품위생안전성학회지
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• 제20권2호
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• pp.77-82
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• 2005

본 연구에서는 식품 단일섭취 또는 식품과 일반의약품으로서의 복합비타민제의 병용섭취를 통해 niacin을 섭취한다는 노출시나리오를 설정하여 우리나라 성인의 niacin 1일 평균섭취량을 산출하였으며, 인체독성자료를 근거로 niacin의 상한섭취량(UL)을 제안하였고 그 값을 비교하여 niacin에 대한 위해지수를 산출하였다. 그 결과 식품 단일섭취 시 위해지수는 0.53,식품과 복합비타민제의 병용섭취 시 위해지수는 0.81-6.24라는 값이 얻어졌다. 일반적으로 위해지수가 1이상이면 건강한 인구집단에서 부작용 발생이 우려됨을 나타낸다 그러므로, 복합비타민제를 병용섭취 하는 일부경우에서는 악영향이 발생할 가능성이 있다고 할 수 있다. 식품을 통한 자연적인 niacin의 섭취로는 악영향이 보고되고 있지 않으나$^{3), 12),}$ 복합비타민제 또는 최근 소비량이 급증하고 있는 비타민 강화 건강기능식품 및 영양보조제 등의 섭취를 통해 niacin으로 인한 악영향의 발생이 우려되므로 지속적이고 세심한 위해성평가와 함께 민감그룹 및 임산부, 수유부 등 특정그룹에 대한 UL설정연구가 이루어져야 할 것으로 생각된다.

• 한국식품영양과학회지
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• 제32권6호
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• pp.806-811
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• 2003

크랜베리 수용액의 색상 안정성 에 대한 pH, 열, 광, 당, 유기산, 금속이온, 비타민 C, $B_1$, $B_3$ 및 $B_{6}$의 영향을 조사하였다. 크랜베리 수용액의 색상은pH가 낮을수록 농색화 효과가 높았고 pH가 높아질수록 최대흡수파장이 장파장 쪽으로 이동하는 bathochromic shift현상이 관찰되었다. 열의 영향에 대한 실험 결과, 색상의 반감기가 37$^{\circ}C$에서 34일, 9$0^{\circ}C$에서 91분, 12$0^{\circ}C$에서 29분으로 온도가 높을수록 색상의 반감기가 급격하게 짧아졌다. 광에 의해 색상의 안정성이 크게 저하되었는데, 형광보다 일광에 대한 영향이 더 컸으며 저장 시 광을 차단함으로써 안정성을 증진시킬 수 있었다. 당류 첨가는 오히려 무첨가구에 비해서 저장 안정성을 저하시켰고 fructose가 색상 저하를 가장 촉진하는 것으로 나타났다. 유기산 중 fumaric acid, citric acid, malic acid, acetic acid 순으로 색상 안정성에 효과가 있었으며 특히 fumaric acid는 색상안정화에 크게 기여하였다. 금속이온 중 $Na^{+}$과 $Mg^{2+}$은 색상안정화에 기여하였으나 $Mn^{2+}$은 색상의 안정성을 가장 크게 저하시켰고 다음으로 F $e^{2+}$, $K^{+}$, $Ca^{2+}$순으로 저하시켰다. 비타민 C와 $B_1$은 크랜베리 수용액 색상의 안정성을 저하시켰으며 특히 비타민 C는 색상의 안정성을 크게 저하시켰다. 반면 $B_3$, $B_{6}$는 색상의 안정성에 미약하게 기여하였다.

• Biomolecules & Therapeutics
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• 제10권3호
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• pp.142-151
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• 2002

The present study was attempted to investigate the effect of apamin on catecholamine (CA) secretion evoked by ACh, high $K^+$, DMPP, McN-A-343, cyclopiazonic acid and Bay-K-8644 from the isolated perfused rat adrenal gland and to establish the mechanism of its action. The perfusion of apamin (1 nM) into an adrenal vein for 20 min produced greatly potentiation in CA secretion evoked by ACh (5.32 $ imes$ $10^{-3}$ M), high $K^+$, (5.6 $ imes$ $10^{-2}$), DMPP ($10^{-4}$ M for 2 min), McN-A-343 ($10^{-4}$ M for 2 min), cyclopiazonic acid ($10^{-5}$ M for 4 min) and Bay-K-8644 ($10^{-5}$ M for 4 min). However, apamin itself did fail to affect basal catecholamine output. Furthermore, in adrenal glands preloaded with apamin (1 nM) under the presence of glibenclamide ($10^{-6}$ M), an antidiabetic sulfonylurea that has been shown to be a specific blocker of ATP-regulated potassium channels (for 20 min), CA secretion evoked by DMPP and McN-A-343 was not affected. However, the perfusion of high concentration of apamin (100 nM) into an adrenal vein for 20 min rather inhibited significantly CA secretory responses evoked by ACh, high $K^+$, DMPP, McN-A-343, cyclopiazonic acid and Bay-K-8644. Taken together, these results suggest that the low concentration of apamin causes greatly the enhancement of CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by membrane depolarization. These findings suggests that apamin-sensitive SK ($Ca^{2+}$) channels located in rat adrenal medullary chromaffin cells may play an inhibitory role in the release of catecholamines mediated by stimulation of cholinergic nicotinic and muscarinic receptors as well as membrane depolarization. However, it is thought that high concentration of apamin cause the inhibitory responses in catecholamine secretion evoked by stimulation of cholinergic receptors as well as by membrane depolarization from the rat adrenal gland without relevance with the SK channel blockade.

• The Korean Journal of Physiology and Pharmacology
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• 제2권2호
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• pp.173-184
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• 1998

The present study was undertaken to examine the influence of glucocorticoids on the secretory responses of catecholamines (CA) evoked by acetylcholine (ACh), DMPP, McN-A-343, excess K^+$ and Bay-K-8644 from the isolated perfused rat adrenal gland and to clarify the mechanism of its action. The perfusion of the synthetic glucocorticoid dexamethasone (10-100\;{\mu}M$) into an adrenal vein for 20 min produced a dose-dependent inhibition in CA secretion evoked by ACh (5.32 mM), excess K^+$ (a membrane-depolarizor 56 mM), DMPP (a selective nicotinic receptor agonist, 100\;{\mu}M$ for 2 min), McN-A-343 (a muscarinic receptor agonist, 100\;{\mu}M$ for 4 min), Bay-K-8644 (a calcium channel activator, 10\;{\mu}M$ for 4 min) and cyclopiazonic acid (a releaser of intracellular $Ca^{2+}$, 10\;{\mu}M$ for 4 min). Similarly, the preperfusion of hydrocortisone (30\;{\mu}M$) for 20 min also attenuated significantly the secretory responses of CA evoked by nicotinic and muscarinic receptor stimulation as well as membrane-depolarization, $Ca^{2+}$ channel activation and the release of intracellular $Ca^{2+}$. Furthermore, even in the presence of betamethasone (30{\mu}M$), CA secretion evoked by ACh, excess K^+$, DMPP and McN-A-343 was also markedly inhibited. Taken together, the present results suggest that glucocorticoids cause the marked inhibition of CA secretion evoked by both cholinergic nicotinic and muscarinic receptor stimulation from the isolated perfused rat adrenal gland, indicating strongly that this inhibitory effect may be mediated by inhibiting influx of extracellular calcium as well as the release of intracellular calcium in the rat adrenomedullary chromaffin cells.

• 한국식품과학회지
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• 제52권2호
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• pp.119-124
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• 2020

본 연구에서는 현사시나무 추출물에 대한 일반성분, 무기질, 비타민, 유리당, 총 페놀과 총 플라보노이드 함량 및 HPLC을 이용하여 페놀성 화합물을 분석하였으며 DPPH, ABTS 라디칼 소거능을 통하여 추출물의 항산화 활성을 조사하였다. 추출물의 일반 성분 분석결과, 탄수화물, 수분, 조단백질, 회분, 조지방은 각각 88.6, 5.11, 2.5, 2.3, 1.5%로 확인되었다. 무기질 분석결과, Ca (77.5 mg/100 g), Mg (85.0 mg/100 g), Na (23.4 mg/100 g), K (907.5 mg/100 g), P (93.8 mg/100 g), Fe (1.4 mg/100 g), Zn (2.6 mg/100 g), Cu (0.6 mg/100 g), Mn (2.9 mg/100 g)을 함유하고 있었다. 비타민의 경우, vitamin C (6.1 mg/100 g), vitamin B₂ (0.3 mg/100 g), vitamin B₆ (0.01 mg/100 g), nicotinic acid (3.1 mg/100 g)가 확인되었다. 유리당 조성은 glucose 1.6%, fructose 2.2%였고 총 페놀 및 총 플라보노이드 함량은 각각 115.4±0.85 mg GAE/g, 20.9±1.14 mg QE/g으로 나타났다. HPLC 분석결과 catechin (9.1±0.27 mg/g), caffeic acid (4.1±0.57 mg/g), p-coumaric acid (2.1±0.47 mg/g), chlorogenic acid (1.6±0.86 mg/g), gallic acid (1.4±0.35 mg/g)가 주요 성분으로 확인되었다. 현사시나무 추출물은 DPPH 및 ABTS 라디칼 소거활성을 보였고 이는 추출물에 함유된 항산화성분에 기인한 것으로 판단되었다. 본 연구에서는 현 사시나무 추출물의 일반성분, 무기질, 비타민, 총 페놀 및 총 플라보노이드 함량, 주요 페놀성 화합물 및 항산화활성을 평가하였지만 향후 현사시나무 추출물이 식품소재 또는 건강기능식품 소재로서 활용 가치를 높이기 위해서는 세포 및 동물모델에서의 바이오마커 평가 및 작용기전 연구가 추가되어야 할 것으로 사료된다.

• Biomolecules & Therapeutics
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• 제15권2호
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• pp.108-117
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• 2007

The aim of the present study was to investigate the effect of glibenclamide, a hypoglycemic sulfonylurea, which selectively blocks ATP-sensitive K$^+$ channels, on secretion of catecholamines (CA) evoked by cholinergic stimulation and membrane depolarization from the isolated perfused rat adrenal glands. The perfusion of glibenclamide (1.0 mM) into an adrenal vein for 90 min produced time-dependently enhanced the CA secretory responses evoked by ACh (5.32 mM), high K$^+$ (a direct membrane depolarizer, 56 mM), DMPP (a selective neuronal nicotinic receptor agonist, 100 ${\mu}$M for 2 min), McN-A-343 (a selective muscarinic M1 receptor agonist, 100 ${\mu}$M for 2 min), Bay-K-8644 (an activator of L-type dihydropyridine Ca$^{2+}$ channels, 10 ${\mu}$M for 4 min) and cyclopiazonic acid (an activator of cytoplasmic Ca$^{2+}$-ATPase, 10 ${\mu}$M for 4 min). In adrenal glands simultaneously preloaded with glibenclamide (1.0 mM) and nicorandil (a selective opener of ATP-sensitive K$^+$ channels, 1.0 mM), the CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were recovered to the considerable extent of the control release in comparison with that of glibenclamide-treatment only. Taken together, the present study demonstrates that glibenclamide enhances the adrenal CA secretion in response to stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by membrane depolarization from the isolated perfused rat adrenal glands. It seems that this facilitatory effect of glibenclamide may be mediated by enhancement of both Ca$^{2+}$ influx and the Ca$^{2+}$ release from intracellular store through the blockade of K$_{ATP}$ channels in the rat adrenomedullary chromaffin cells. These results suggest that glibenclamide-sensitive K$_{ATP}$ channels may play a regulatory role in the rat adrenomedullary CA secretion.

• The Korean Journal of Physiology and Pharmacology
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• 제5권2호
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• pp.189-197
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• 2001

To investigate propofol's effects on ionic currents induced by ${\gamma}-aminobutyric$ acid (GABA) and glycine as well as on those produced by the nicotinic acetylcholine- and glutamate-responsive channels, rat dorsal raphe neurons were acutely dissociated and the nystatin-perforated patch-clamp technique under voltage-clamp conditions was used to observe their responses to the administration of propofol. Propofol evoked ion currents in a dose-dependent manner, and propofol $(10^{-4}\;M)$ was used to elicit ion currents through the activation of $GABA_A,$ glycine, nicotinic acetylcholine and glutamate receptors. Propofol at a clinically relevant concentration $(10^{-5}\;M)$ potentiated $GABA_A-,$ glycine- and NMDA receptor-mediated currents. The potentiating action of propofol on $GABA_A-,$ glycine- and NMDA receptor-mediated responses involved neither opioid receptors nor G-proteins. Apparently, propofol modulates inhibitory and excitatory neurotransmitter-activated ion channels either by acting directly on the receptors or by potentiating the effects of the neurotransmitters, and this modulation appears to be responsible for the majority of the anaesthetic and/or adverse effects.

• Natural Product Sciences
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• 제13권1호
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• pp.68-77
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• 2007

The aim of the present study was to examine the effects of green tea extract (CUMS6335) on the release of CA evoked by cholinergic stimulation and direct membrane-depolarization in the perfused model of the adrenal gland isolated from the spontaneously hypertensive rats (SHRs), and to establish the mechanism of action. Furthermore, it was also to test whether there is species difference between animals, and between CUMS6335 and EGCG, one of biologically the most powerful catechin compounds found in green tea. CUMS6335 $(100\;{\mu}g/ml)$, when perfused into an adrenal vein for 60 min, time-dependently inhibited the CA secretory responses evoked by ACh (5.32mM), high $K^+$(56 mM), DMPP $(100\;{\mu}M)$, and McN-A-343 $(100\;{\mu}M)$ from the isolated perfused adrenal glands of SHRs. However, CUMS6335 itself did fail to affect basal catecholamine output. Also, in adrenal glands loaded with CUMS6335 $(100\;{\mu}g/ml)$, the CA secretory responses evoked by Bay-K-8644 $(10\;{\mu}M)$ and cyclopiazonic acid $(10\;{\mu}M)$ were also inhibited in a relatively time-dependent fashion. However, in the Presence of EGCG $(8.0\;{\mu}g/ml)$ for 60 min, the CA secretory response evoked by ACh, high $K^+$, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were not affected except for last period. Collectively, these results indicate that CUMS6335 inhibits the CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by direct membrane-depolarization from the perfused adrenal gland of the SHR. It seems that this inhibitory effect of CUMS6335 is exerted by blocking both the calcium influx into the rat adrenal medullary chromaffin cells and the uptake of $Ca^{2+}$ into the cytoplasmic calcium store, which are at least partly relevant to the direct interaction with the nicotinic receptor itself. It seems likely that there is much difference in mode of the CA-releasing action between CUMS6335 and EGCG.

• KSBB Journal
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• 제11권6호
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• pp.636-641
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• 1996

김치발효 중에 분리한 젖산균의 일종인 Leueonos toe sp. KY -002를 이용하여 mannitol 생산 특성을 검토하였다. 여러 가지 탄소원 중에서 설탕과 과당만 이 mannitol 생성의 기질로 이용되었고, 50 g/L 과 당을 기질로 사용할 경우 mannitol 생산성이 가장 좋 았으며 이때 최대수율은 초기과당 기준으로 약 52% 이었다. 초기 탄소원이 고갈펼 경우, 생성된 manmtol이 다시 기질로 이용되지 않았고, 100 ~ 250 g/L 이상의 고놓도 기질농도에서는 수율이 30% 이하 수 준으로 낮았으나, 모든 실험조건에서 다른 탕알콜류 를 부산물로 생성하지 않았다. Mannitol 생성에 미 치는 여러 가지 배양인자들을 검토한 결과, 질소원 으로 yeast extract가 가장 우수하였고, 무기인산염 은 10 g/L 농도 벙위까지 농도가 높을수록 유리하 였으며, 금속이온과 NaCI, KCl 등의 엽류의 천가는 m mannitol 발효에서 역효과를 나타내였다. 몇 가지 vitamin류의 첨가에 의해 mannitol 생산을 촉진시 킬 수 있었는데, 특히 nicotinic acid의 첨가에 의해 발효놓도를 16% 증가시킬 수 있었다. 배양환경중 온도는 $35^{\circ}C$, 초기 pH는 6이 최적이었다.