• YAKHAK HOEJI
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• v.33 no.1
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• pp.64-71
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• 1989

Since time-dependent inactivation of MAO was found to be complete in a few minutes when high concentration ratios of tranylcypromine to MAO were used, a method to obtain kinetic parameters was sought suitable to the conditions in which concentrations of tranylcypromine analogs did not exceed that of MAO. For the purpose, kinetic equations were derived and the method applied to the kinetic studies of tranylcypromine enantiomers. It was found that (E)-(+)-2-phenylcyclopropylamine inhibited MAO by the mechanism following bimolecular reaction scheme with $\tilde{K}_i$ of $2.0\;{\times}\;10^6M^{-1}min^{-1}$. Whereas, MAO-inhibitory pattern of the (-)-enantiomer was to be interpreted by suicide inhibition scheme and measured $k_{in}\;and\;\tilde{K}'$ were $0.457\;min^{-1}\;and\;$5.4{\mu}M$, respectively.

• Archives of Pharmacal Research
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• v.9 no.2
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• pp.99-110
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• 1986

In order to use for metabolic studies of tranylcypromine (TCP), TCP-phenyl-$d_{5}$ was synthesized via the intermediates, 3-benzoylpropionic acid-$d_{5}$ and trans-2-phenylcyclopropanecarboxylic acid-$d_{5}$ -TCP(0.22 mmole/kg) and its deuterated analog were administered s. c. to the rats and GC/MS analyses of the urines led to the detection of N-acetyltranylcypromine (ATCP) and glucuronide conjugate of phenyl-hydroxylated ATCP. MAO activities in rat brain were measured using serotonin as the substrate. In vitro $IC_{50}$ of ATCP was determined to be $10^{-3}M$. The inhibitions by ATCP were not dependent on the preincubation time and were reversed by washing sedimented mitochondrial pellets after the preincubation. In vivo MAO inhibitions at various times of 0.5, 1.5, 3, 6, 12, and 23 hr after the administration of 0.4 mmole/kg (i. p. ) of ATCP were found to be 0.13, 73, 90, 89, and 74 %, respectively. Similarly, the inhibition percents by 0.015 mmole/kg (i. p. ) of TCP were 94, 99, 95, 91, 71 and 49%. The results strongly suggest that deacetylated product of ATCP may account for its in vivo MAO inhibition. The relationship between the metabolism via phenyl-hydroxylation and the in vivo potency of TCP was examined by QSAR study and it was found that groupings discriminating between the compounds with p-substituents and those without them only ensure high correlations, suggesting that ring-hydroxylation which occurs at the para position in most of the compounds is a determining factor to the potency of TCP.

• Natural Product Sciences
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• v.19 no.4
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• pp.281-285
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• 2013

This study was designed to investigate the nervous sedative effects of green tea. The sedative effect was evaluated by examination of Monoamine oxidases (MAOs) inhibitory activity in vitro in the brain and liver of rat fed on green tea cultivated and harvested from the different regions and periods. It showed that methanol extracts of green tea inhibited significantly the brain MAO-A activity. Especially late harvested green tea extracts showed potential inhibitory activity. The liver MAO-B activity was also inhibited by all of the green tea extracts with strong intensity. This study confirmed that major compounds of green tea such as catechin, epigallocatechin-3-gallate (EGCG) and L-theanine, which were well known for the main bioactive components in the tea plants, were not associated with the MAO inhibitory activities of green tea. These results suggested that a MAO inhibition activity comes from other minor tea components we have to search in the future.

• Archives of Pharmacal Research
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• v.10 no.2
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• pp.142-147
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• 1987

Fourteen kinds of medicinal plants were screened for determining inhibitory activities on monoamine oxidase B. The extracts of Artemisia Messer-Schmidtiana (herba), Chrysanthemum indicum(flos), Ericibe obtusifolia (radix et rhizoma) and Sophora japonica (flos) strongly inhibited the enzyme. Among them, Chrysanthemi flos was chosen for elucidating its active principles, and some flavonoids were isolated and identified as acasetin (I), 5, 7-dihydroxy chromone (II), diosmetin (III), apigenin (IV), eriodictyol (V) and luteolin (VI).$IC_{50} were determined as following: 1, 2.46;II, 0.19; III, 2. 11mM, and the others showed weak inhibition.

• YAKHAK HOEJI
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• v.42 no.1
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• pp.101-107
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• 1998

The antiparkinsonian agent l-deprenyl, a selective monoamine oxidase (MAO)-B inhibitor, is metabolized in part to l-methamphetamine and l-amphetamine. l< /I>-Deprenyl was evaluated for amphetamine and methamphetamine-like discriminative stimulus effects in rats and its mechanism of action was investigated. Rats were trained under a 5-response, fixed ratio schedule of stimulus-shock termination or a 10-response. Fixed-ratio schedule of food-presentation which discriminate between d-amphetamine (1mg/kg, i.p.) and saline or d-methamphetamine (1mg/kg, i.p.) and saline in a two-lever, operant conditioning procedure. Full generalization was obtained to d-amphetamine (1~3mg/kg). d-methamphetamine (1~3mg/kg) and l-deprenyl (17~30mg/kg) under both the food presentation and stimulus shock termination schedule. l-Deprenyl has dose-dependent amphetamine-and methamphetamine-like discriminative stimulus properties in rats only at doses of 17 and 30mg/kg. Reversible MAO-B inhibitor, RO 16-6491 didn`t show any amphetamine-like discriminative properties. Aromatic amino acid decarboxylase inhibitor, NSD 1015 decreased % responding of l-deprenyl in the methamphetamine-trained rats under the stimulus-shock termination schedule. SKF-525A produced partial inhibition of methamphetamine-like discriminative effects of l-deprenyl under the food presentation schedule. These results suggest that l-deprenyl has no abuse liability at the therapeutic range but there needs some caution at high doses and furthermore, drug discrimination studies under the food presentation and shock termination schedule are useful for the assessment of abuse liability of psychostimulants.

• Food Science of Animal Resources
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• v.38 no.3
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• pp.615-628
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• 2018

Preserved egg, a kind of alkaline-fermented food, is a traditional egg product in China. Here, we investigated the nutritional functions of preserved eggs by in vivo and in vitro experiments. The results of in vivo studies showed that the levels of triglycerides (TG), total cholesterol (TCHO) and low-density lipoprotein cholesterol/high density lipoprotein cholesterol (LDL-C/HDL-C) were significantly decreased (p<0.05) in the liver of rats treated with preserved eggs. Meanwhile, the levels of two important cancer markers, interleukin-6 (IL-6) and tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$), were also significantly decreased (p<0.05) in treated rats. In vitro studies were performed on Caco-2 cells, a human epithelial colorectal adenocarcinoma cell line. It demonstrated that the gastrointestinal (GI) digests of preserved eggs significantly accelerated (p<0.05) the apoptosis by upregulating caspase-3 in the Caco-2 cells. Besides, after treated with preserved eggs, the half maximal inhibitory concentration (IC50) of preserved eggs digests to Caco-2 cells was 5.75 mg/mL, indicating the significant inhibition of cell proliferation provided by preserved eggs (p<0.05). The results shown in this study demonstrated that preserved eggs may be a novel functional food involved with antilipemic, anti-inflammatory activity as well as the effect on accelarating the apoptosis of Caco-2 cells.

• Journal of Oral Medicine and Pain
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• v.38 no.4
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• pp.313-318
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• 2013

The aim of this study was to the relationship between sleep disturbances and Burning mouth syndrome(BMS). BMS presents as a chronic burning sensation in the oral mucous membrane that is frequently associated with sleep disturbances. BMS is considered neuropathic pain condition with dysfunction of small diameter afferent sensory fiber. A review of the studies reveals, BMS suggested peripheral and cental nervous system changes. Sleep disruption or Rem sleep deprivation cause an inhibition of opioid protein synthesis and a reduced affinity of ${\mu}$ and ${\delta}$ opioid receptors. Let me say that sleep disturbances suggest a risk factor For BMS and support to evaluate as a part of BMS treatment. Further study will be required to ascertain the relationship between distruption of sleep continuity or Rem sleep deprivation and BMS and the evidence of altered neurochemical degeneration of BMS.