• Biomolecules & Therapeutics
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• 제14권2호
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• pp.102-105
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• 2006

We examined the effects of psoralen derivatives on a rapidly activating delayed rectifier $K^+$ channel (hKv1.5) cloned from human heart and stably expressed in $Ltk^-$ cells. Using the whole cell configuration of the patch-clamp technique, we found that the five psoralen derivatives inhibited hKv1.5 current. Especially, 4-(2-Propenyloxy)-7H-furo[3,2-g][1]benzopyran-7-one (compound 5) was more potent than the inhibition of the hKv1.5 current of psoralen. The compound 5 inhibited the hKv1.5 current in a concentration-, time-, and voltage-dependent manner. These results suggest that the compound 5 is an excellent candidate as an antiarrhythmic drug for atrial fibrillation.

• Archives of Pharmacal Research
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• 제28권3호
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• pp.269-273
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• 2005

A furocoumarin derivative, psoralen (7H-furo[3,2-g][1]benzopyran-7-one), was isolated from the n-hexane fraction of Heracleum moellendorffii Hance. We examined the effects of psor-alen on a human Kv1.5 potassium channel (hKv1.5) cloned from human heart and stably expressed in Uk- cells. We found that psoralen inhibited the hKv1.5 current in a concentration-, use- and voltage-dependent manner with an IC$_{50}$ value of 180 $\pm$ 21 nM at +60 mV. Psoralen accelerated the inactivation kinetics of the hKv1.5 channel, and it slowed the deactivation kinetics of the hKv1.5 current resulting in a tail crossover phenomenon. These results indicate that psoralen acts on the hKv1.5 channel as an open channel blocker. Furthermore, psoralen prolonged the action potential duration of rat atrial muscles in a dose-dependent manner. Taken together, the present results strongly suggest that psoralen may be an ideal antiarrhythmic drug for atrial fibrillation.

• Archives of Pharmacal Research
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• 제25권5호
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• pp.664-668
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• 2002

KR-31543,(2S,3R,4S)-6-amino-4-[N-(4-chlorophenyl)-N-(2-methyl-2H-tetrazol-5-ylmethyl)amino]-3,4-dihydro-2-dimethoxymethyl-3-hydroxy-2-methyl-2H-1-benzopyran is a new neuroprotetive agent for ischemia-reperfusion damage. The in vitro and in vivo metabolism of KR-31543 in rats has been studied by LC-electrospray mass spectrometry. Rat liver microsomal incubation of KR-31543 in the presence of NADPH resulted in the formation of a metabolite M1. M1 was identified as N-(4-chlorophenyl)-N-(2-methyl-2H-tetrazol-5-ylmethyl)amine on the basis of LC-MS/MS analysis with the synthesized authentic standard. Rat CYP3A1 and 3A2 are the major CYP isozymes involved in the formation of M1.

• Preventive Nutrition and Food Science
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• 제6권4호
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• pp.230-234
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• 2001

The extract of Ulmus davidiana var. japonica cortex has known as natural anti-inflammatory substance in East Asia. For the identification of antimicrobial substance, it was extracted by using methanol and fractionated by using different organic solvents. The fraction of butanol was represented the highest antimicrobial activities. Therefore, the butanol fraction was purified and identified the chemical structure by $^1$H and $^{13}$ C-NMR spectra, FT-IR and EI/MS spectroscopies. The isolated antimicrobial substance was identified as cis-2-[3,4-dihydroxy phenyl]-3,4-dihydro-2H-1-benzopyran-3,5,7-triol, which has commonly known as (-)epicatechin. Its minimum inhibitory concentrations (MICs) against Staphylococcus aureus and Listeria monocytogenes were shown as 100 $\mu\textrm{g}$/mL, respectively.

• Archives of Pharmacal Research
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• 제26권8호
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• pp.606-611
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• 2003

Byakangelicin, 9-(2,3-dihydroxy-2-methylbutoxy)-4-methoxy-7H- furo[3,2-g][l]benzopyran-7-one (BKG), a component of Angelicae dahuricae Radix, is considered to be an inhibitor of aldose reductase for the treatment of diabetic cataract. An analytical method for the isolation of BKG developed by high-performance liquid chromatography has been reported. No literature on the metabolism of BKG, however, has been found. With the purpose of identifying new metabolites of BKG, BKG (100 mg/kg) was orally administered to Sprague-Dawley rats via a gavage. Using a metabolic cage, urine was collected for 24 h, and the urine samples were extracted by liquid-liquid extraction. For structural identification of new urinary metabolites of BKG, various instrumental analyses were conducted by gas-chromatography/mass spectrometry, high-performance liquid chromatography/diode array detector, liquid chromatography/mass spectroscopy with thermospray interface and $^1H$ nuclear magnetic resonance spectroscopy. Two metabolites produced from the Ο-demethylation or Ο-dealkylation of BKG were newly identified, and another new but unknown metabolite was assumed to be the hydroxylated form of BKG. These results indicate that the major metabolic products of BKG are formed by Ο-demethylation or Ο-dealkylation of BKG side chains.

• 한국융합학회논문지
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• 제9권4호
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• pp.75-84
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• 2018

본 연구는 서울에서 유통되는 식품용 융합 환제에 대하여 위해물질인 벤조피렌 등의 PAHs (polycyclic aromatic hydrocarbons) 오염실태를 조사하고 위해도를 평가하였다. 2010~2013년 서울약령시 한약재 판매업소 등에서 31종 93건의 환제를 수집한 후 시료를 추출, 여과, 농축하여 SPE (Sep-pak florisil)로 유출시킨 후 다시 농축하여 액체크로마토그래프로 분석하였다. 분석한 결과 총 8종 PAHs 평균 함량은 $10{\mu}g/kg$ 이하이었고, PAHs 위해성 평가 결과 초과발암위해도는 일상 생활에서의 노출에 의한 것보다 낮았고, 노출안전역(MOEs)은 대부분의 시료가 위해를 무시할 만한 수준으로 안전한 것으로 평가되었다. 향후 의약용 환제와 식품용 환제의 위해물질에 대한 비교 융합연구가 필요하다.

• Journal of Forest and Environmental Science
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• 제33권2호
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• pp.113-121
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• 2017

In flight particulate matter particularly emissions generated by incomplete combustion processes has become a subject of global concern due to the health problems and environmental impacts associated with them. This has compelled most countries to set standards for coarse and fine particles due to their conspicuous impacts on environment and public health. This contribution therefore explores forest fire emissions and how its particulates affects air quality, damage to vegetation, water bodies and biological functions as architects for lung diseases and other degenerative illnesses such as oxidative stress and aging. Soot was collected from simulated forest fire using a clean glass surface and carefully transferred into amber vials for analysis. Volatile components of soot were collected over 10 mL dichloromethane and analyzed using a QTOF Premier-Water Corp Liquid Chromatography hyphenated to a mass selective detector (MSD), and Gas Chromatograph coupled to a mass spectrometer (GC-MS). To characterize the size and surface morphology of soot, a scanning electron microscope (SEM) was used. The characterization of molecular volatiles from simulated forest fire emissions revealed long chain compounds including octadec-9-enoic acid, octadec-6-enoic acid, cyclotetracosane, cyclotetradecane, and a few aromatic hydrocarbons (benzene and naphthalene). Special classes of organics (dibenzo-p-dioxin and 2H-benzopyran) were also detected as minor products. Dibenzo-p-dioxin for instance in chlorinated form is one of the deadliest environmental organic toxins. The average particulate size of emissions using SEM was found to be $11.51{\pm}4.91{\mu}m$. This study has shown that most of the emissions from simulated forest fire fall within $PM_{10}$ particulate size. The molecular by-products of forest fire and particulate emissions may be toxic to both human and natural ecosystems, and are possible precursors for various respiratory ailments and cancers. The burning of a forest by natural disasters or man-made fires results in the destruction of natural habitats and serious air pollution.

• Biomolecules & Therapeutics
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• 제22권4호
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• pp.275-281
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• 2014

Autophagy is a series of catabolic process mediating the bulk degradation of intracellular proteins and organelles through formation of a double-membrane vesicle, known as an autophagosome, and fusing with lysosome. Autophagy plays an important role of death-survival decisions in neuronal cells, which may influence to several neurodegenerative disorders including Parkinson's disease. Chebulagic acid, the major constituent of Terminalia chebula and Phyllanthus emblica, is a benzopyran tannin compound with various kinds of beneficial effects. This study was performed to investigate the autophagy enhancing effect of chebulagic acid on human neuroblastoma SH-SY5Y cell lines. We determined the effect of chebulagic acid on expression levels of autophagosome marker proteins such as, DOR/TP53INP2, Golgi-associated ATPase Enhancer of 16 kDa (GATE 16) and Light chain 3 II (LC3 II), as well as those of its upstream pathway proteins, AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR) and Beclin-1. All of those proteins were modulated by chebulagic acid treatment in a way of enhancing the autophagy. Additionally in our study, chebulagic acid also showed a protective effect against 1-methyl-4-phenylpyridinium ($MPP^+$) - induced cytotoxicity which mimics the pathological symptom of Parkinson's disease. This effect seems partially mediated by enhanced autophagy which increased the degradation of aggregated or misfolded proteins from cells. This study suggests that chebulagic acid is an attractive candidate as an autophagy-enhancing agent and therefore, it may provide a promising strategy to prevent or cure the diseases caused by accumulation of abnormal proteins including Parkinson's disease.

• 한국응용곤충학회지
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• 제35권3호
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• pp.238-242
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• 1996

몇가지 협력제의 7-ethoxy precocene II와 협력작용을 통한 활성증가와 작용기작을 구명하기 위하여 mikweed bug, Oncopeltus fasciatus 2령충에 항유약호르몬유사물과 협력제가 처리된 petri dish에 접종하여 생리활성 정도를 측정하였다. 얻어진 결과는 다음과 같다. 7-Ehtoxy precocene II의 반수활성농도는 $1.18\mu$g/$\textrm{cm}^2$이었다. 7-Ethoxy precocene II와 다른 산화저해제인 RO20-9747의 협력비가 14.05로 가장 높았고 그들의 반수활성농도는 $0.084\mu$$g/\textrm{cm}^2$이었다. 7-Ethoxy precocene II와 다른 협력제 1종, 2종, 4종을 조합을 달리하여 처리하였을 때 뚜렷한 협력작용 증가효과를 가져오지 못했다. 이상의 결과에서 다른 협력제들은 곤충의 방어기작을 알라타체를 포함하여 비선택적으로 저해하는 것으로 생각되었으나 RO20-9747은 7-ethoxy precocene II가 알라타체로 이행하는데 까지 곤충의 방어적 산화기작인 monooxygenase 활성을 선택적으로 저해함으로써 7-ethoxy precocene II가 알라타체로 이행량이 증가하여 활성증가를 가져온 것으로 생각되었다.

• The Korean Journal of Physiology and Pharmacology
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• 제14권5호
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• pp.257-263
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• 2010

Visnagin (4-methoxy-7-methyl-5H-furo[3,2-g][1]-benzopyran-5-one), which is an active principle extracted from the fruits of Ammi visnaga, has been used as a treatment for low blood-pressure and blocked blood vessel contraction by inhibition of calcium influx into blood cells. However, the neuroprotective effect of visnagin was not clearly known until now. Thus, we investigated whether visnagin has a neuroprotective effect against kainic acid (KA)-induced neuronal cell death. In the cresyl violet staining, pre-treatment or post-treatment visnagin (100 mg/kg, p.o. or i.p.) showed a neuroprotective effect on KA ($0.1{\mu}g$) toxicity. KA-induced gliosis and proinflammatory marker (IL-$1{\beta}$, TNF-${\alpha}$, IL-6, and COX-2) inductions were also suppressed by visnagin administration. These results suggest that visnagin has a neuroprotective effect in terms of suppressing KA-induced pathogenesis in the brain, and that these neuroprotective effects are associated with its anti-inflammatory effects.