• Korea Journal of Cosmetic Science
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• 제1권1호
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• pp.31-43
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• 2019

Melanosomes are specific melanin-containing intracellular organelles of epidermal melanocytes. In epidermal melanocytes, there are three kinds of key player proteins. Rab27a, melanophilin or Slac2-a and Myosin 5a form a tripartite complex connects the melanosome. Mature melanosomes make movements through the tripartite protein complex along actin filaments.In this study, we found that the haplamine (6-Methoxyflindersine) induced melanosome aggregation around the nucleus in epidermal melanocyte. In an attempt to elucidate the inhibitory effect of haplamine on melanosome transport, effect of haplamineon the expression level of Rab27a, melanophilin and Myosin 5a was measured. The results indicated that haplamine up to 5��M effectively suppressed mRNA and protein expression level of melanophilin.To determine the upstream regulator of melanophilin regulated by haplamine, we checked the level of MITF, c-JUN and USF1. Those are possible transcription factor of melanophilin. Among them,treatment of USF1 siRNA decreased mRNA and protein expression level of USF1 as well as melanophilin. Also, treatment of haplamine decreased mRNA and protein expression level of melanophilin as well as USF1 in a dose-dependent manner. Consequently, we found the inhibitory effect of haplamine on melanosome transport in melan-a melanocyte. Treatment of haplamine reduced melanophilin expression level which is a key protein of melanosome transport. We identified that USF1 could be a major transcription factor of melanophilin regulated by haplamine.

• BMB Reports
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• 제30권2호
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• pp.157-161
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• 1997

The present paper reports characteristics and specificity of the inhibitory action of $N^{\alpha}-tosyl-L-lysine-chloromethyl\;ketone$ (TLCK) and $N^{\alpha}-tosyl-L-phenylalanine-chloromethyl\;ketone$ (TPCK) on the glucose6-phosphate transporter of rat liver microsomes. The TLCK-induced inhibition was pH dependent. The inhibition constants for TPCK were determined by following pseudo-Lst order reaction mechanism. The inhibition was protected by preincubation with excess amount of glucose-6-phosphate. The results proved that (a) TLCK inactivates the microsomal glucose-6-phosphate transporter, (b) the inhibition results from the modification of sulfhydryl groups of the transporter.

• The Korean Journal of Physiology
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• 제10권2호
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• pp.1-10
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• 1976

The action of acetylcholine on the sodium plus potassium activated ATPase activity in the rabbit red cell membrane has been investigated and the experiments were also designed to determine the mechanism of action of acetylcholine on the ATPase activity. The following results were observed. 1. The activity of the NaK ATPase from red cell membrane is inhibited by acetylcholine. 2. The ratio of inhibition of NaK ATPase by acetylcholine is decreased by raising the potassium concentration, and is increased by raising the sodium concentration. 3. The ATPase activity is increased by small amounts of calcium but inhibited by larger amounts. The ratio of inhibition of the enzyme by acetylcholine is increased by raising the calcium concentration. 4. The inhibitory action of acetylcholine on the NaK ATPase activity was not related to the sulfhydryl group of cysteine, the hydroxyl group of threonine, or the carboxyl group of aspartic acid. 5. The inhibitory action of acetylcholine on the ATPase activity is due to amino group of the enzyme of NaK ATPase.

• Bulletin of the Korean Chemical Society
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• 제29권1호
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• pp.43-46
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• 2008

The aim of present study was to examine the inhibitory effects of hydroxamic acid derivatives on the melanogenesis. We found that hydroxamic acid moiety was important for anti-melanogenic activity. Compounds 1a and 1b strongly inhibited melanin synthesis via deactivation of tyrosinase. Hydroxamic acid has metal ion chelating ability which is similar to that kojic acid, however, anti-tyrosinase mechanism of compounds 1a and 1b was different from that of kojic acid. They showed noncompetitive inhibition kinetics

• 한국생물공학회:학술대회논문집
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• 한국생물공학회 2005년도 생물공학의 동향(XVII)
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• pp.821-826
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• 2005

Postprandial hyperglycemia plays an important role in the development of type 2 diabetes and complications associated with the disease such micro-and macro-vascular disease. The present study investigated the effect and action mechanism of a ethanolic extract from the Schizandra chinensis(SC-E) on hypeglycemia in vivo and in vitro. In vitro, SE-E demonstrated a potent inhibitory effects on ${\alpha}-amylase$ activity ($IC_{50}$ : 4 ${\mu}g/ml$). Its inhibition on ${\alpha}-amylase$ was determined to be competitive type. Oral administration of SE-E markedly lowered plasma glucose levels in non-fasted streptozotocin induced diabetic rats (45 mg/kg BW). In addition when it was orally administrated to rats with starch (2g/kg BW), SC-E (50 and 100 mg/kg BW) significantly suppressed the increase of blood glucose levels after starch loading . These results suggest that some edible plants merit further evaluation for clinical usefulness as anti-diabetic drugs.

• 한방안이비인후피부과학회지
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• 제17권1호
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• pp.94-103
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• 2004

Objective: This study was performed to detennine the depigmenting effects of Kamibongpungtongsung-San. Methods: To determine the depigmenting effects of Kamibangpungtongsung-San. we measured the degree of tyrosinase inhibition, melanin production & cell viability in cultured B16 melanoma cells, UV screen and cytoprotective effects on PC12 cells injured by hydrogen peroxide. Results: Komibangpungtongsung-San did not show inhibitory effects on melanin production in melanoma cells, UV screen and cytoprotective effects on PC12 cells injured by hydrogen peroxide. However it showed mild inhibitory effects on tyrosinase activity. Conclusion : This study shows that Kamibangpungtongsung-San, a generally used prescription for dermatologic diseases, do not have depigmenting effects via tyrosinase inhibition. Therefore, the depigmenting effect and mechanism of depigmentation by Kamibangpungtongsung-San need to be evaluated and investigated in other directions.

• 대한화학회지
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• 제14권2호
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• pp.161-168
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• 1970

In order to obtain the more effective evidence, supporting the hypothesis which have been previously described by former report that pepsin (EC 3.4. 4.1) forms a hydrophobic bond with the nonpolar side chain of its substrate, the inhibitory effect of carboxylic acids(from formic acid to iso-butyric acid) on the activity of pepsin to the synthetic dipeptide, N-Carbobenzoxy-L-glutamyl-L-tyrosine, was discussed. The kinetic study showed that the inhibition by carboxylic acids was competitive. The Kidecreased with increasing size of the inhibitor molecule. The $-{\Delta}F^{\circ}$increased linearly with increasing number of carbon atoms in the hydrocarbon chain of the inhibitor. It was confirmed that the hydrophobic bond between more than one side chain of amino acid residues(phenylalanine) in the binding region of the active center of pepsin and the side chain of amino acid residues in the substrate was formed as the first step of its enzymic mechanism. The inhibitory effect of carboxylic acids was due to the competition of the hydrocarbon group of the carboxylic acids with the side chain of the substrate for the hydrophobic binding site(the side chain of phenylalanine) of the pepsin.

• 생약학회지
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• 제46권1호
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• pp.1-5
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• 2015

In the course of screening tyrosinase inhibitory activity, EtOAc-soluble fraction of Nelumbinis Semen (Seeds of Nelumbo nucifera) showed significant inhibition. Further fractionation of the EtOAc-soluble fraction resulted in 12 compounds, which were identified as 4-(hydroxymethyl)phenol (1), tyrosol (2), 4-(hydroxymethyl)benzaldehyde (3), 4-hydroxybenzoic acid (4), 4-(2-methoxyvinyl)benzene-1,2-diol (5), 2,6-dihydroxybenzoic acid (6), (2R-trans)-2,3-dihydro-3,5,7,8-tetrahydroxy-2-(4-hydroxyphenyl)-4H-1-benzopyran-4-one (7), (+)-catechin (8), elephantorrhizol (9), (+)-dehydrovomifoliol (10), (-)-boscialin (11) and uridine (12). Compounds 5 and 7 were first reported from this plant. Among the isolated compounds, compound 7 showed strong inhibition on tyrosinase activity with mixed mechanism of competitive and noncompetitive inhibition.

• BMB Reports
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• 제51권1호
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• pp.3-4
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• 2018

Parkinson's disease (PD) is a debilitating disorder resulting from loss of dopamine neurons. In dopamine deficient state, the basal ganglia increases inhibitory synaptic outputs to the thalamus. This increased inhibition by the basal ganglia output is known to reduce firing rate of thalamic neurons that relay motor signals to the motor cortex. This 'rate model' suggests that the reduced excitability of thalamic neurons is the key for inducing motor abnormalities in PD patients. We reveal that in response to inhibition, thalamic neurons generate rebound firing at the end of inhibition. This rebound firing increases motor cortical activity and induces muscular responses that triggers Parkinsonian motor dysfunction. Genetic and optogenetic intervention of the rebound firing prevent motor dysfunction in a mouse model of PD. Our results suggest that inhibitory synaptic mechanism mediates motor dysfunction by generating rebound excitability in the thalamocortical pathway.

• 약학회지
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• 제43권5호
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• pp.659-664
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• 1999

To investigate the difference of contractile mechanism between KCI and phenylephrine-induced contraction, we observed effects of $Ca^{2+}$ antagonists and protein kinase inhibitors on aorta contraction of rats. Verapamil dose-dependently inhibited the contraction induced by KCI and phenylephrine, the inhibitory effect of verapamil was more potent in KCI-induced contraction than phenylephrine-induced contraction. Econazole and TMB-8 significantly inhibited CKI-induced contraction but did not inhibit phenylephrine-induced contraction. Staurosporine dose-dependently inhibited both KCI and phenylephrine-induced contraction. Genistein and calmodulin antagonists (W-7 and trifluoperazine) also inhibited both contraction in a dose dependent manner. However, the inhibitory effects of genistein and calmodulin antagonists were more potent in phenylephrine-induced contraction than KCI-induced contraction. These results suggest that involvements of $Ca^{2+}$ channel and protein kinase in rat aorta contraction were dependent on agonist causing aorta smooth muscle contraction.