Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Pyrones”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,495 records · Page 83Linked to original sources
PubMed2001

Composition of the essential oil of two Nepeta species and in vitro evaluation of their activity against Helicobacter pylori.

The chemical composition of the essential oils obtained from the aerial parts of Nepeta camphorata and Nepeta argolica ssp. dirphya were analysed by GC-MS. A total of 52 components were identified and significant differences (qualitative and quantitative) were observed between the two samples. 1,8-Cineol and two nepetalactones were found to be the major components of the oil of N. camphorata and N. argolica ssp. dirphya respectively. The in vitro activity, of the two oils and the three above mentioned isolated compounds, against 25 clinically isolated and commercial strains of Helicobacter pylori was investigated and some activity was found.

Cyclohexanols↗
PubMed2002

The skin-lightening effects of artocarpin on UVB-induced pigmentation.

This study was conducted to evaluate the effects of the prenylated flavonol artocarpin from the heartwood of Artocarpus incisus on ultraviolet (UV)-induced hyperpigmentation of guinea pig skin. An efficient lightening effect was observed following topical application of artocarpin to UV-stimulated hyperpigmented dorsal skins of brownish guinea pigs.

Animals↗
PubMed2002

Kavain attenuates vascular contractility through inhibition of calcium channels.

Kavain is a biologically active compound from the Oceanic plant Piper methysticum (kava). Traditional medicinal uses of the kava root are many. Kava is increasingly being utilized by Western societies for its anxiolytic effects. Recent reports indicate that kavain blocks ion channels in neural tissue, relaxes precontracted ileum, and relaxes precontracted airway. Thus, we investigated the potential ability of this plant-derived compound to alter vascular smooth muscle function. Thoracic aortae were isolated from Sprague-Dawley rat and cut into 4 mm rings. Rings were placed in tissue baths and suspended from force-displacement transducers for the measurement of isometric tension. In a dose-dependent manner, kavain (10(-6) M to 10(-3) M) was found to relax aortic rings precontracted with phenylephrine (PE). This response was not dependent on functional endothelium. In addition, kavain pretreatment (3 x 10(-5) M or 3 x 10(-4) M) attenuated vascular smooth muscle contraction evoked by PE. However, kavain failed to attenuate PE-mediated contraction in calcium (Ca(++))-free buffer, indicating that intracellular signaling processes were likely not affected. Also, kavain did attenuate the contraction elicited by administration of Ca(++) to depolarized tissue. Interestingly, in rings pre-treated with the selective L-type Ca(++) channel blocker nifedipine, kavain-mediated relaxation was inhibited. Lastly, in rings selectively contracted with an L-type calcium channel activator, kavain elicited dose-dependent (and ultimately complete) relaxation. These data strongly suggest that kavain impairs vascular smooth muscle contraction, likely through inhibition of Ca(++) channels.

Animals↗
PubMed2002

Mechanisms of relaxant action of a pyranocoumarin from Peucedanum japonicum in isolated rat thoracic aorta.

The CHCl(3) -soluble fraction obtained from the MeOH extract of Peucedanum japonicum Thunb. inhibited phenylephrine-induced vasoconstriction in isolated rat thoracic aorta. We isolated a vasorelaxing compound, as one of the bioactive components, which was identified as (+)- cis-4'- O-acetyl-3'- O-angeloylkhellactone (1), a pyranocoumarin, and examined the mechanisms of vasorelaxant effect caused by 1. This compound (1) (10(-6)-10(-4) M) concentration-dependently relaxed the isolated rat thoracic aorta pre-contracted with phenylephrine (PE). This vasorelaxant potency was diminished by endothelial removal (by 20%), L- N(G)-nitro-arginine or methylene blue (MB), but not indomethacin treatment. These findings indicate that the vasorelaxant effect of 1 was partially endothelium dependent and mediated by nitric oxide and cyclic GMP pathway. To determine if the effect of 1 was mediated through the activation of some of the receptors known to lead to vascular relaxation, the effects of atropine, triprolidine and propranolol were determined. 1-induced vasorelaxation was not affected by atropine, triprolidine and propranolol. Compound 1 inhibited high potassium (80 mM)-induced, calcium-dependent contractions in a concentration-dependent manner. But it slightly relaxed the rat aorta precontracted with PE in the presence of nifedipine, a blocker of voltage-operated calcium channels. Tetraethylammonium (TEA, a non-specific (K+) channel blocker) did not affect the vasodilatory effect of 1 against PE-induced contraction. Mechanisms of the vasorelaxant effect of 1 were multiple, including endothelium dependence and Ca(2+) channel blockade.

Animals↗
PubMed2002

Kavalactones and dihydrokavain modulate GABAergic activity in a rat gastric-brainstem preparation.

Using an in vitro neonatal rat gastric-brainstem preparation, the activity of majority neurons recorded in the nucleus tractus solitarius (NTS) of the brainstem were significantly inhibited by GABA A receptor agonist, muscimol (30 microM), and this inhibition was reversed by selective GABA A receptor antagonist, bicuculline (10 microM). Application of kavalactones (300 microg/ml) and dihydrokavain (300 microM) into the brainstem compartment of the preparation also significantly reduced the discharge rate of these NTS neurons (39 % and 32 %, respectively, compared to the control level), and this reduction was partially reversed by bicuculline (10 microM). Kavalactones or dihydrokavain induced inhibitory effects were not reduced after co-application of saclofen (10 microM; a selective GABA B receptor antagonist) or naloxone (100 nM; an opioid receptor antagonist). Pretreatment with kavalactones (300 microg/ml) or dihydrokavain (300 microM) significantly decreased the NTS inhibitory effects induced by muscimol (30 microM), approximately from 51 % to 36 %. Our results demonstrated modulation of brainstem GABAergic mechanism by kavalactones and dihydrokavain, and suggested that these compounds may play an important role in regulation of GABAergic neurotransmission.

Animals↗
PubMed2002

Inhibition of cytochrome P450 3A4 by extracts and kavalactones of Piper methysticum (Kava-Kava).

Inhibitors of cytochrome P450 3A4 (CYP3A4) were identified in crude extracts from the rhizomes of Piper methysticum G. Forst. (Kava-Kava) using bioassay-guided fractionation. After preliminary purification of an ethyl acetate extract with solid phase extraction, the eluate was further fractionated by means of HPLC and fractions were tested for inhibitory potency using cDNA expressed CYP3A4. Positive fractions were analysed with LC/MS using electrospray ionisation and kavapyrones could be identified as the main CYP3A4 inhibitory components of Piper methysticum.

Anisoles↗
PubMed2003

Kinobeon A as a potent tyrosinase inhibitor from cell culture of safflower: in vitro comparisons of kinobeon A with other putative inhibitors.

Kinobeon A is produced from cell cultures of the medicinal plant, safflower. Mushroom tyrosinase activity was inhibited in a concentration-dependent manner when treated with kinobeon A using L-tyrosine or L-3,4-dihydroxyphenylalannine (L-DOPA) as substrates. IC50 values were 22 microM (substrate: L-tyrosine) and 27 microM (L-DOPA). Inhibition of human tyrosinase activity also increased with increasing concentrations of kinobeon A using L-DOPA as the substrate, with an IC50 value of 2.5 microM. Kinobeon A was a more potent competitive inhibitor than kojic acid, arbutin or L-ascorbic acid for both mushroom and human tyrosinase as determined from Lineweaver-Burk plots. These results suggested that kinobeon A could be a potent natural tyrosinase inhibitor.

Agaricales↗
PubMed2003

Prenylated flavonoids from the roots of Sophora flavescens with tyrosinase inhibitory activity.

Prenylated flavonoids containing the resorcinol moiety were isolated as tyrosinase inhibitors from the roots of Sophora flavescens by activity-guided fractionation. Among the 12 compounds isolated, kuraridin, kurarinone and norkurarinol showed stronger inhibitory potencies (IC 50 = 1.1, 1.3 and 2.1 microM, respectively) than that of kojic acid (IC 50 = 11.3 microM), a well known tyrosinase inhibitor. Substitution of a lavandulyl or hydroxylavandulyl group at the C-8 position and a methoxy or hydroxy group at the C-5 position are essential for the inhibitory effect.

Flavonoids↗
PubMed2004

Streptozotocin-induced alterations in rat liver Golgi complexes are ameliorated by BMOV [Bis(maltolato)oxovanadium(IV)] activity.

Twenty years ago, we detected the interdependence between structure and function of rat liver Golgi complexes that are characteristic for streptozotocin diabetes, which served us in further investigations as a useful indicator of the effectiveness of drugs we were testing. This work presented results obtained in eight groups of rats (four control and four diabetic) that were administered orally either bis(maltolato)oxovanadium(IV) [BMOV] or maltol alone. The activities of the rat liver Golgi marker enzyme, galactosyltransferase [GalT], as well as the morphology of Golgi complexes were studied in situ using an electron microscope; parallel estimations of vanadium concentration and phospholipid percentage were made in Golgi-rich preparations isolated from the liver. Our main findings were normalization in diabetic animals orally treated with 1.8 mmol BMOV in 0.09 mol NaCl solutions over seven days, which demonstrated an accompanying increase in phosphatidic acid (PA) percentage (p < 0.05) compared to controls. In the diabetic groups, Pearson's test showed a positive double correlation between GalT activity, vanadium concentration, and PA percentage in Golgi-rich membrane preparations from the liver. Additionally, a negative correlation was found between vanadium concentration and phosphatidylcholine percentage in the fractions.

Animals↗
PubMed2004

A beta-secretase (BACE1) inhibitor hispidin from the mycelial cultures of Phellinus linteus.

In the course of screening for anti-dementia agents from natural products, a beta-secretase (BACE1) inhibitor was isolated from the culture broth of Phellinus linteus and identified as hispidin. It showed an IC (50) value of 4.9 x 10 (-6) M and a Ki value of 8.4 x 10 (-6) M. The compound was a non-competitive inhibitor. Hispidin also inhibited a prolyl endopeptidase (IC (50) = 1.6 x 10 (-5) M, Ki = 2.4 x 10 (-5) M), but it was less inhibitory to alpha-secretase (TACE) and other serine proteases such as chymotrypsin, trypsin, and elastase.

Alzheimer Disease↗
PubMed2004

Kava does not display metabolic toxicity in a homogeneous cellular assay.

To determine whether kava (Kava kava, 'Awa, Yaqona, Piper methysticum Forst.), the popular herbal product associated recently with possible human hepatotoxicity, is bioactivated by cytochrome P450 enzymes to cytotoxic metabolites, three kava lactones (methysticin, yangonin, and desmethoxyyangonin) and an ethanolic extract of dried kava root were incubated over time in culture with MCL-5 cells, a human lymphoblastoid cell line that has been stably transfected with five human P450's (CYP 1A1, 1A2, 2A6, 2E1, and 3A4) and human epoxide hydrolase. Incubations were performed concurrently with a control cell line (cH2) that is derived from the same parental line as MCL-5, but transfected with two empty vectors. The kava compounds displayed varying degrees of toxicity (IC (50) values ranged from 50 to > 100 microM) to the MCL-5 and cH2 cell lines; however, both cell lines were equally sensitive to the test compounds. These results suggest that the parent compound for each of the four test compounds was primarily responsible for the observed cell toxicity and that CYP 1A1, 1A2, 2A6, 2E1, and 3A4 or epoxide hydroxylase did not appear to be involved. Thus, in vitro kava does not appear to be activated to toxic metabolites by enzymes known to be important in metabolic toxicity.

Cell Line↗
PubMed2004

Pyranocoumarin(+/-)-4'-O-acetyl-3'-O-angeloyl-cis-khellactone induces mitochondrial-dependent apoptosis in HL-60 cells.

The pyranocoumarin (+)-4'-O-acetyl-3 'O-angeloyl-cis-khellactone (PC) isolated from Radix Peucedani (root of Peucedanum praeruptorum Dunn) showed a dose-dependent effect at 10 -30 pg/mL on causing apoptotic DNA and nuclear fragmentations in HL-60 cells. After 24 h of PC treatment there were losses of mitochondrial membrane potential and cytochrome c. PC also increased total cellular and mitochondrial Bax protein, stimulated an increase in caspase-dependent Bcl-2 cleavage but showed no effect on Bcl-Xv. These observations strongly suggest activation of the mitochondria apoptotic pathway. The pan-specific caspase inhibitor, ZVAD-fmk, abolished the PC-induced apoptosis,whereas the caspase-8 inhibitor IETD-fmk showed no effect, implying the involvement of the caspase 9 pathway. PC caused a 2 to 12 hour transient increase in phospho-ERK, and a 72 h-long activation of JNK. Pre-treatment with the MEK inhibitor PD98059, which suppresses ERK activation, paradoxically promoted PC-induced mitochondrial cytochrome c release, procaspase-3 and -8 cleavage, and enhanced apoptosis. Our results show that PC triggers mitochondria-mediated apoptosis in HL-60 cells, and the involvement of ERK and JNK signal pathways in the process.

Antineoplastic Agents, Phytogenic↗
PubMed1998

Influence of genuine kavapyrone enantiomers on the GABA-A binding site.

The influence of kavapyrones from Piper methysticum Forst. on the GABAA receptor was demonstrated using radioreceptor assays. Both the dienolide yangonin and the genuine enolide enantiomers (+)-kavain, (+)-dihydrokavain, (+)-methysticin, and (+)-dihydromethysticin enhanced the specific binding of [3H]bicuculline methochloride ([3H]BMC). The kavapyrones have been investigated at assay concentrations between 100 microM and 10 nM. (+)-Kavain, (+)-methysticin and (+)-dihydromethysticin showed maximal enhancements of 18% to 28% at a concentration of 0.1 microM, whereas a 100-fold concentration of (+)-dihydrokavain revealed a similar modulatory activity of 22%. In the presence of 1 microM yangonin an increase of about 21% of the specific [3H]BMC binding was observed. Desmethoxyyangonin did not alter the binding behavior of the GABAA-receptor. A structure comparison of desmethoxyyangonin and yangonin indicated that the aromatic methoxy group was of particular importance for the modulatory activity. In contrast, the substitution pattern of the aromatic ring did not influence the modulatory activity of the enolides in a decisive manner. A structure comparison of desmethoxyyangonin and (+)-kavain revealed that an angular lactone ring was an important structure requirement. Both the enolides and the dienolides did not inhibit the specific binding of [3H]flunitrazepan. Thus, the influence on the GABAA receptor was not based upon an interaction of these kavapyrones with the benzodiazepine receptor.

Animals↗
PubMed1998

In vivo effects of the kavapyrones (+)-dihydromethysticin and (+/-)-kavain on dopamine, 3,4-dihydroxyphenylacetic acid, serotonin and 5-hydroxyindoleacetic acid levels in striatal and cortical brain regions.

The in vivo effect of a single oral dose of 100 mg (+)-dihydromethysticin/kg body weight on striatal and cortical tissue concentrations of dopamine, serotonin, 3,4-dihydroxyphenylacetic acid and 5-hydroxyindoleacetic acid, as well as the dopamine and serotonin turnover, was tested in rats. Additionally, other rats were fed with a (+/-)-kavain containing food over a period of 78 days in order to calculate the influence of a chronic treatment with kavapyrones on the neurotransmitters. The results of the present in vivo study clearly demonstrate that neither (+)-dihydromethysticin in a high single dose, nor (+/-)-kavain chronically administered, altered the dopaminergic or serotonergic tissue levels in rats significantly.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1997

In vitro antimutagenic effects of anthraquinone aglycones and naphthopyrone glycosides from Cassia tora.

The antimutagenic activity of a methanol extract of Cassia tora seeds against aflatoxin B1(AFB1) was demonstrated with the Salmonella typhimurium assay. The numbers of revertants per plate decreased significantly when this extract was added to the assay system using Salmonella typhimurium TA100 and/or TA98. The MeOH extract was then sequentially partitioned with CH2Cl2, n-BuOH and H2O. The CH2Cl2 and n-BuOH fractions possessed antimutagenic activity but the H2O fraction was inactive. Neither the MeOH extract nor its fractions were capable of inhibiting the direct-acting mutagen N-methyl-N'-nitro-N-nitrosoguanidine suggesting that these fractions may prevent the metabolic activation of AFB1 or scavenge the electrophilic intermediate capable of inducing mutations. Column chromatography using silica gel yielded pure chrysophanol, chryso-obtusin, and aurantio-obtusin from the CH2Cl2 fraction and cassiaside and rubro-fusarin gentiobioside from the n-BuOH fraction. Each of these compounds demonstrated significant antimutagenic activity.

Animals↗
PubMed1997

Cytotoxicity and electron microscopy of cell death induced by goniothalamin.

The cytotoxicity of goniothalamin was found to be strong towards both cancerous (HGC-27, MCF-7, PANC-1, HeLa), and non-cancerous (3T3) cell lines, especially in cases of dividing cells. Drug exposure studies indicated that the cytotoxic action of goniothalamin was time- and dose-dependent. At the ultrastructural level, goniothalamin-induced cytotoxicity revealed a necrotic mode of cell death towards MCF-7 cells.

3T3 Cells↗
PubMed1997

Aged garlic extract and its constituents inhibit Cu(2+)-induced oxidative modification of low density lipoprotein.

Oxygen radical injury and lipid peroxidation have been suggested as major causes of atherosclerosis, cancer, liver disease, and the aging process. More specifically, oxidative modification of low density lipoprotein (LDL) has been recognized as an important process of atherosclerosis. In this study, we determined the effects of aged garlic extract (AGE), four of its constituents, and a metabolite on Cu(2+)-induced oxidative modification of LDL using an in vitro system. All these compounds were shown to inhibit oxidative modification of LDL.

Antioxidants↗