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Results for “Polyunsaturated Alkamides”

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At least 19 recordsLinked to original sources
PubMed1994

In vitro inhibition of cyclooxygenase and 5-lipoxygenase by alkamides from Echinacea and Achillea species.

Polyunsaturated alkamides isolated from Achillea species, Echinacea angustifolia DC., Anacyclus pyrethrum (L.) Link, and Aaronsohnia pubescens (Desf.) Bremer & Humphries, (Compositae) were shown to possess inhibitory activity in in vitro cyclooxygenase (sheep seminal microsomes) and 5-lipoxygenase (porcine leukocytes) assays. Activity appeared to depend on the particular structure of the alkamides.

Amides↗
PubMed2007

Alkamide stability in Echinacea purpurea extracts with and without phenolic acids in dry films and in solution.

Degradation of the major alkamides in E. purpurea extracts was monitored under four different accelerated storage conditions, phenolic-depleted and phenolic-rich dry E. purpurea extracts and phenolic-depleted and phenolic-rich DMSO E. purpurea extracts at 70, 80, and 90 degrees C. Degradation of alkamides followed apparent first-order reaction rate kinetics. Alkamides degraded faster in dry films than in DMSO solution. The phenolic acids acted as antioxidants by limiting the loss of the alkamides in dry E. purpurea extracts. In contrast, E. purpurea alkamides in DMSO degraded faster when the phenolic fraction was absent. The overall order of degradation rate constants was alkamides 1 approximately 2 approximately 6 > 9 approximately 8 > 3 approximately 5 approximately 7. The energy of activation (Ea) predicted for alkamide degradation averaged 101 +/- 12 kJ/mol in dry films +/- phenolic acids, suggesting the oxidation mechanism was the same under both conditions. In DMSO solutions, Ea values were about one-half of those in dry films (61 +/- 14 kJ/mol), suggesting a different mechanism for alkamide oxidation in solution compared to dry. Predicted half-lives for alkamides in extracts suggested very good stability.

Dimethyl Sulfoxide↗
PubMed2004

Isolation and synthesis of isodihydropiperlonguminine.

The hexane extract of dried fruits of Piper longum on fractionation afforded a new alkamide, isodihydropiperlonguminine and two phenyl propanoic acid derivatives. The structures of these compounds are established based on spectroscopic evidence and synthesis.

Fruit↗
PubMed2002

Transport of alkamides from Echinacea species through Caco-2 monolayers.

To gain more insights into the human intestinal absorption of alkamides from Echinacea species, transport studies were performed with the human adenocarcinoma colonic cell line Caco-2 (ATCC) as a model to assess the epithelial transport of dodeca-2 E,4 E,8 Z,10 E/ Z-tetraenoic acid isobutylamides (1/ 2). 30 minutes after apical loading of 25 microg/ml 1/ 2, about 15 % of these alkamides were detectable on the basolateral side. Close monitoring of the transport during 6 hours revealed a nearly complete transport to the basolateral side after 4 hours and no significant metabolism was observable. Transport experiments performed at 4 degrees C showed only a slight decrease in transport, which is a strong hint that dodeca-2 E,4 E,8 Z,10 E/ Z-tetraenoic acid isobutylamides (1/ 2) cross biological membranes by passive diffusion. Nearly the same results were obtained after preincubation of the Caco-2 cells with lipopolysaccharides (LPS) or phorbol 12-myristate-13-acetate (PMA) to mimic an inflammatory status. These results support the assumption that the alkamides can be easily transported from the intestinum and hence may contribute to the in vivo effects of Echinacea preparations.

Biological Transport↗
PubMed2005

Macrophage activating effects of new alkamides from the roots of Echinacea species.

Chemical investigation of the roots of Echinacea angustifolia, E. purpurea, and E. pallida yielded two new alkamides, identified by analysis of spectroscopic data and comparison with reported alkamides. The new compounds were dodeca-2Z,4E,10Z-trien-8-ynoic acid isobutylamide (1) from E. angustifolia and dodeca-2Z,4E-diene-8,10-diynoic acid isobutylamide (2) from E. purpurea and E. pallida. These two components, as well as previously identified alkamides, exerted inhibition on LPS-mediated activation of a murine macrophage line, RAW264.7. These data suggest that these alkamides may have anti-inflammatory activity. The cytotoxicity of these alkamides using MTT assays was also investigated.

Amides↗
PubMed2004

Fungistatic and bacteriostatic activities of alkamides from Heliopsis longipes roots: affinin and reduced amides.

This work demonstrates the fungistatic and bacteriostatic activities of affinin, the main alkamide of Heliopsis longipes (Gray) Blake (Asteraceae) roots and two alkamides obtained by catalytic reduction of affinin: N-isobutyl-2E-decenamide and N-isobutyl-decanamide. The bioactivity was tested against Rhizoctonia solani groups AG3 and AG5, Sclerotium rolfsii, Sclerotium cepivorum, Fusarium sp., Vertcillium sp., phytopathogenic fungi; Phytophthora infestans, a phytopathogenic Chromista; Saccharomyces cerevisiae, a nonphytopathogenic ascomycete; and Escherichia coli, Erwinia carotovora, and Bacillus subtilis, bacteria. Affinin, being the primary component of the lipidic fraction, is expected to be responsible for the fungitoxic activity observed in roots of this plant species. Four of the assayed fungi showed an important sensitivity to the presence of affinin: S. rolfsii, S. cepivorum, P. infestans, and R. solani AG-3 and AG-5, displaying a growth inhibition of 100%. S. cerevisiaeshowed a similar growth inhibition with affinin. None of the alkamides obtained by catalytic reduction of affinin showed a fungitoxic activity. Affinin had a definite negative effect on the growth of E. coli and B. subtilis, but E. carotovora carotovora was not sensitive to the highest dose of affinin assayed. N-Isobutyl-2E-decenamide displayed a higher bacteriostatic activity against E. coli and E. carotovora carotovora. In both cases, this alkamide was more potent than affinin. On the other hand, only N-isobutyl-decanamide displayed a significant activity on the growth of B. subtilis.

Alkenes↗
PubMed2005

Bioavailability and pharmacokinetics of alkamides from the roots of Echinacea angustifolia in humans.

Alkamides are suspected to contribute to the activity of Echinacea preparations. They are mainly derived from undeca- and dodecanoic acid and differ in the degree of unsaturation and the configuration of the double bonds. In total, 6 alkamides have been isolated from the roots of Echinacea angustifolia as major lipophilic constituents and have been investigated regarding their pharmacokinetics. A sensitive and specific method has been developed for the identification and quantification of these alkamides in human plasma using liquid chromatography electrospray ionization ion-trap mass spectrometry. The method was applied to analyze plasma samples obtained from a randomized, open, single-dose, crossover study after oral administration of a 60% ethanolic extract from the roots of E. angustifolia to 11 healthy subjects. The maximum concentration of dodeca-2E,4E,8Z,10E/Z-tetraenoic acid isobutylamides, the main alkamides in the roots of E. angustifolia, appeared already after 30 minutes and was 10.88 ng/mL for the 2.5-mL dose.

Administration, Oral↗
PubMed1999

Effect of temperature on stability of marker constituents in Echinacea purpurea root formulations.

Stability of an alkamide and a phenolic phytochemical marker in a hydro-alcoholic extract of Echinacea purpurea root and a dried powder prepared by evaporation of the extract was assessed in storage for 7 months at three temperature regimes: -20, 25 and 40 degrees Celsius. In the extract, the major alkamide, dodeca-2E, 4E, 8Z, 10E/Z-tetraenoic acid isobutyl amide, was not significantly affected by storage at any of the temperatures, but cichoric acid content declined as significantly (P = 0.05) at both 25 degrees C and 40 degrees C as compared to low-temperature storage. In the powder, the major alkamide showed a significantly reduced level at 25 degrees C and 40 degrees C while cichoric acid did not decline significantly. These results suggest that more attention should be given to the effect of formulation and temperature on storage of Echinacea products.

Caffeic Acids↗
PubMed2002

Simultaneous analysis of alkamides and caffeic acid derivatives for the identification of Echinacea purpurea, Echinacea angustifolia, Echinacea pallida and Parthenium integrifolium roots.

A reversed-phase HPLC method was developed using a computer simulation program for the identification of dried roots of Echinacea purpurea, E. angustifolia, E. pallida and Parthenium integrifolium. Hydrophilic and lipophilic compounds were analysed simultaneously leading to a two-fold decrease in analysis time compared to traditional HPLC methods.

Asteraceae↗
PubMed2001

Absorption of dodeca-2E,4E,8Z,10E/Z-tetraenoic acid isobutylamides after oral application of Echinacea purpurea tincture.

Alkamides are suspected to contribute to the activity of Echinacea preparations. In preliminary experiments a quantification method for dodeca-2E,4E,8Z,10E/Z-tetraenoic acid isobutylamides in human blood has been developed by which it was possible to detect dodeca-2E,4E,8Z,10E/Z-tetraenoic acid isobutylamides in human blood after oral application of Echinacea purpurea mother tincture.

Administration, Oral↗
PubMed2002

Constituents of Lepidium meyenii 'maca'.

The tubers of Lepidium meyenii contain the benzylated derivative of 1,2-dihydro-N-hydroxypyridine, named macaridine, together with the benzylated alkamides (macamides), N-benzyl-5-oxo-6E,8E-octadecadienamide and N-benzylhexadecanamide, as well as the acyclic keto acid, 5-oxo-6E,8E-octadecadienoic acid. The structure elucidation of the isolated compounds was based primarily on 1D and 2D NMR spectroscopic analyses, including 1H-1H COSY, 1H-13C HMQC, 1H-13C HMBC and 1H-1H NOESY experiments, as well as from 1H-15N NMR HMBC correlations for macaridine and N-benzylhexadecanamide.

Amides↗
PubMed2005

Alkamides from the leaves of Zanthoxylum syncarpum.

Three alkamides (1-3) were isolated from the leaves of Zanthoxylum syncarpum. The structures of the new compounds 1 and 2 were established by spectroscopic data and chemical conversion, and by the X-ray crystallography of 1. Compound 3, the racemic form of the known compound syncarpamide, showed moderate antiplasmodial activity, with IC50 values of 4.2 and 6.1 microM against Plasmodium falciparum D6 clone and W2 clone, respectively.

Animals↗
PubMed2006

Analgesic activity of affinin, an alkamide from Heliopsis longipes (Compositae).

Heliopsis longipes (Compositae) is a Mexican plant used as analgesic in pain toothache. A solution of 10mug/ml of dichloromethane extract from this plant showed analgesic activity determined by means of GABA release in mice brain slices. Through a bioassay-directed separation, fractions G-1, G-2, G-4 and G-6 at the same concentration were active. Affinin was the unique and common active compound, and evoke the GABA release 0.5min after administration at 1x10(-4)M concentration. Inactive compound were undeca-2E-en-8,10-dyinoic acid isobutylamide, hinokinin, 2'-hydroxyhinokinin, 3beta-sn-glyceroyl-(1''-palmitoxy)urs-12-ene, 13(18)-ursen-3beta-ol, 13(18)-ursen-3beta-acetate, beta-sitosterol and stigmasterol. The analgesic activity of Heliopsis longipes could be associated to affinin.

4-Butyrolactone↗
PubMed2006

ACAT inhibition of alkamides identified in the fruits of Piper nigrum.

In this study, via a bioactivity-guided fractionation of MeOH extracts of the fruits of Piper nigrum, alkamide (5) and five previously-identified alkamides were isolated. Their structures were elucidated via spectroscopic analysis ((1)H, (13)C NMR and ESI-MS), as follows: retrofractamide A (1), pipercide (2), piperchabamide D (3), pellitorin (4), dehydroretrofractamide C (5) and dehydropipernonaline (6). The IC(50) values determined for the compounds were 24.5 (1), 3.7 (2), 13.5 (3), 40.5 (4), 60 (5) and 90 microM (6), according to the results of an ACAT enzyme assay system using rat liver microsomes. These compounds all inhibited cholesterol esterification in HepG2 cells.

Amides↗
PubMed1996

Inhibition of cell growth of human hepatoma cell line (Hep G2) by a farnesyl protein transferase inhibitor: a preferential suppression of ras farnesylation.

So far, treatment with anti-cancer agents has failed to achieve satisfactory results in hepatocellular carcinoma. In the process of hepatocarcinogenesis, ras has been shown to play a role. ras requires a farnesyl moiety for activation. It has been found that UCFI-C (manumycin), an antibiotic, inhibits farnesyl protein transferase, an enzyme that catalyzes farnesylation. Therefore, we investigated the effects of UCFI-C on cell growth, prenylation of cellular proteins including ras and Rapl, MAP kinase activity, activities of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and synthesis of cholesterol in a ras-activated human hepatoma cell line, Hep G2. Treatment with varying concentrations of UCF1-C(10-30 microM for 24 and 72 hr resulted in a time- and dose-dependent inhibition of cell numbers. 3H-Thymidine incorporation was also inhibited in a dose-dependent manner, with 50% inhibition after 44 hr being observed at a concentration of 17 microM. UCFI-C dose-dependently inhibited ras farnesylation and MAP kinase activity, but did not decrease Rap 1++ geranylgeranylation or prenylation of 21-to 26-kDa proteins. Neither the activities of 3-hydroxy-3-methylglutaryl-coenzyme A reductase nor cholesterol synthesis were inhibited. These results suggest that UCFI-C antagonizes the growth of Hep G2 via the suppression of ras farnesylation and could be a lead for the development of new anti-cancer agents blocking the function of oncogenic ras associated with human cancer, including hepatocellular carcinoma.

Alkyl and Aryl Transferases↗
PubMed1997

17beta-estradiol, diethylstilbestrol, tamoxifen, toremifene and ICI 164,384 induce morphological transformation and aneuploidy in cultured Syrian hamster embryo cells.

To examine the ability of estrogens and anti-estrogens to induce cellular transformation and genetic effects, Syrian hamster embryo (SHE) cells were treated with estrogens, 17beta-estradiol (E2) or diethylstilbestrol (DES), or with anti-estrogens, tamoxifen (TAM), toremifene (TOR) or ICI 164,384. Treatment with each substance for 1-3 days suppressed cellular growth in a dose-dependent manner. Colony-forming efficiency (CFE) increased following treatment of cells with E2 or DES for 48 hr at 3 or 10 microM but decreased at 20 or 30 microM. In contrast, CFE was increased by treatment with TAM, TOR or ICI 164,348 over the concentration range examined (1-30 microM). Treatment with each chemical at 1-30 microM for 48 hr caused morphological transformation of SHE cells in a dose-related fashion. The highest frequency was exhibited in SHE cells treated with DES at 20 microM and was 2 times higher than that induced by treatment with benzo[alpha]pyrene (B[alpha]P) at 4 microM. Transformation frequencies induced by other substances (E2, TAM, TOR and ICI 164,348) did not exceed that induced by the B[alpha]P treatment. TOR showed a higher transforming ability over all concentrations examined when compared to the other anti-estrogens (TAM and ICI 164,348). No significant increases in the frequencies of chromosomal aberrations were observed in SHE cells that were treated with any of the chemicals. However, treatment of SHE cells with each chemical induced a dose-dependent increase of aneuploid cells in the near diploid range. Our results indicate that the ability of the estrogens and anti-estrogens to induce numerical chromosomal abnormality may be involved in their cell transformation activity and potential carcinogenicity.

Aneuploidy↗
PubMed1997

Different points of action of retinoids and anti-estrogens in G1 phase identified in synchronized T-47D breast cancer cells.

Both retinoids and anti-estrogens inhibit breast cancer cell proliferation with accumulation of cells in the G1 phase of the cell cycle, but the effect of retinoids is delayed compared to that of anti-estrogens. To determine whether this temporal difference is due to a simple delay in the action of retinoids on a common site or to different sites of action within the G1 phase, we studied the cell cycle effects of retinoic acid (RA) and the anti-estrogen ICI 164384 (ICI) in T-47D cells partially synchronized by mevalonic acid rescue of lovastatin-induced cell cycle arrest. We found that cells entering the cell cycle semi-synchronously after mevalonic acid rescue of lovastatin treatment were immediately susceptible to ICI but not RA. This suggests that RA may act at a point up-stream and ICI at a point down-stream of lovastatin action. Consistent with this, cells recommencing cell cycle progression after RA treatment were susceptible to the effects of lovastatin, while cells pre-treated with ICI then rescued with estradiol were not. In addition, cells rescued from cell cycle arrest induced by either RA, ICI or lovastatin entered S phase with the same kinetics. Our findings suggest, first, that within G1, RA acts before and ICI acts after the point of lovastatin action and, second, that despite these differences in the initiation of cell cycle arrest, the final nature of the cell cycle arrest is similar. Hence, retinoids and anti-estrogens may be expected to target different cell cycle-regulatory molecules to initiate cell cycle arrest, while overcoming this arrest may be accomplished by the activation of a common molecular pathway.

Cell Cycle↗