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PubMed2005

Curcuminoid ligands for sensitization of near-infrared lanthanide emission.

Fluorescent lanthanide complexes were synthesized using a non-phenolic analog of curcumin as the principal chromophoric chelating ligand. Sensitized, near-infrared fluorescence is observed in these complexes as a result of photo-excitation of the chromophoric ligands, population of the molecular triplet state, and transfer of energy to the emitting lanthanide ion. For the purpose of intra-molecular energy transfer, the triplet states of curcuminoid ligands are more favorably matched with the excited electronic states of neodymium and ytterbium ions than those associated with less conjugated beta-diketonate ligands. Sensitization of fluorescence through an internal redox reaction, thought to occur in other ytterbium complexes, is predicted to be less probable under the present circumstances.

Journal Article↗

PubMed1996

Inhibitory effects of alkyl gallate and its derivatives on fatty acid desaturation.

Alkyl gallate, which is known as an antioxidant, intensively inhibited delta 5 and delta 6 desaturation in both rat liver microsomes and an arachidonic acid-producing fungus Mortierella alpina 1S-4. The rat liver microsomal delta 5 and delta 6 desaturases were inhibited by gallic acid esterified with alcohols with various numbers of carbons, suggesting that the necessary structure in an esterified alcohol for the inhibition is not so strict. Among the three hydroxy groups in gallic acid, the m-hydroxy group was shown to be the necessary structure. Kinetic analyses revealed that propyl gallate is a noncompetitive inhibitor of delta 5 desaturase (Ki = 2.6.10(-5)M) and delta 6 desaturase (Ki = 1.7.10(-4) M). These data indicate that alkyl gallate is a new type of desaturase inhibitor and different from known natural inhibitors, i.e., sesamin and curcumin.

Animals↗

PubMed1993

Effects of flavonoids on the release of reactive oxygen species by stimulated human neutrophils. Multivariate analysis of structure-activity relationships (SAR).

In the present study we measured the inhibition by 34 compounds, either flavonoids or related substances, of the release of reactive oxygen species by human neutrophils after stimulation by three agents: the bacterial peptide N-fMetLeuPhe (FMLP), the protein kinase C activator phorbol myristate acetate (PMA) or opsonized zymosan (OZ), using two chemiluminescent probes, lucigenin or luminol in the presence or absence of horseradish peroxidase (HRP). The data matrix (34 x 7) was submitted to multivariate analysis: first, a correspondence factorial analysis to uncover levels of correlation among the biochemical parameters and the specificity of action of the test-compounds and second, a minimum spanning tree analysis that classified the chemical structures into a network describing both specificity and amplitude of the inhibition of the chemiluminescence response. The major conclusions of the analyses were: (a) opposition between inhibition of poly-morphonuclear leukocytes (PMNs) stimulated by FMLP and of PMNs stimulated by PMA or OZ implying that, for the molecules under study, there was a fundamental difference in the manner in which this inhibition occurred and, conversely, a difference in the nature of the stimulatory action of these activators. Molecules lacking hydroxyl groups on ring B, i.e. chrysin, chalcone, flavone and galangin, molecules glycosylated in position 7, i.e. hesperidin and naringin and ring B mono-hydroxylated molecules were, for the most part, at the origin of this dichotomy and might interfere with the membrane FMLP receptor; (b) a marked difference in chemiluminescence inhibition in the presence or absence of HRP that can be explained by the differential action of catechins compared to flavone and flavonol derivatives; (c) a similarity in biological profile between non-flavonoids such as chalcone and phloretin and low mean-activity flavonoids such as chrysin and galangin and between the non-flavonoid curcumin and the highly active flavonoid isorhamnetin; (d) a reaffirmation of the importance of ring A (C5,7) and ring B (C3',4') dihydroxylation, ring C (C3) hydroxylation, but also of the presence of a methoxy group on ring B in engendering high potency. This potency is generally decreased by C2-C3 saturation and by glycosylation. The most active molecules identified in this study provide valuable information for the selection of simpler molecules (e.g. metabolites accounting for the potency of orally administered flavonoids) for further structure-activity relationship (SAR) studies that could lead to the design of novel drugs or prodrugs.

Acridines↗

PubMed1992

Screening for chemopreventive (anticarcinogenic) compounds in rodents.

The Chemoprevention Branch is testing dozens of candidate chemopreventive compounds in the following rodent model carcinogenesis systems: mouse skin papillomas, DMBA/TPA induced, rat mammary adenocarcinoma, DMBA and MNU induced, hamster tracheal squamous cell carcinoma, MNU induced, and lung adenocarcinoma, DEN induced, rat and mouse colon adenocarcinoma, AOM and MAM acetate induced, respectively, and mouse bladder carcinoma, hydroxy BBN induced. Significant chemopreventive (i.e., anticancer) effects have been produced with 4-hydroxy-phenylretinamide, difluoromethylornithine, piroxicam, oltipraz (a dithiolthione), calcium glucarate, N-acetylcysteine, beta-carotene, ibuprofen, dehydroepiandrosterone (DHEA) and a 16-fluoro DHEA analog, 8354, tamoxifen, glycyrrhetinic acid, molybdate, selenite, curcumin, and fumaric acid.

Animals↗

PubMed1994

Experimental databases on inhibition of the bacterial mutagenicity of 4-nitroquinoline 1-oxide and cigarette smoke.

Two antimutagenicity databases were prepared by applying a co-treatment procedure to the Salmonella reversion assay. Ninety compounds belonging to various chemical classes were quantitatively tested for antimutagenicity towards the direct-acting mutagen 4-nitroquinoline 1-oxide (4NQO) in strain TA100 of S. typhimurium and 63 of them were additionally tested for antimutagenicity towards unfractionated mainstream cigarette smoke (CS) in strain TA98, in the presence of S9 mix. Twelve compounds (13.3%) inhibited 4NQO mutagenicity by at least 50%, with a MID50 (dose inhibiting 50% of mutagenicity) varying over a 1226-fold range. Twenty-six compounds (41.3%) inhibited CS mutagenicity, with a MID50 varying over a 520-fold range. Three compounds only, i.e., bilirubin, curcumin and myricetin, were capable of inhibiting the mutagenicities of both 4NQO and CS. However, myricetin and the other flavonoid rutin were at the same time mutagenic by inducing frameshift mutations following metabolic activation. There was a rather rigorous selectivity of antimutagenicity data depending on the chemical class of inhibitors and it was possible to discriminate protective effects within several pairs or series of structurally related compounds. For instance, all eight thiols and aminothiols inhibited 4NQO mutagenicity, which contrasted with the inactivity of the remaining 17 sulfur compounds tested, all of them lacking a free sulfhydryl group. The mutagenicity of CS was consistently inhibited by the majority of phenols (eight out of 10 tested) and by all two isothiocyanates, two dithiocarbamates, three indole derivatives, three tetrapyrrole compounds and three flavonoids tested. Although the results obtained cannot be extrapolated to other mutagens or test systems, they may provide a useful source of information for research in the area of antimutagenesis and for the development of chemopreventive agents.

4-Nitroquinoline-1-oxide↗

PubMed1983

The active part of the [6]-gingerol molecule in mutagenesis.

A study was performed to discover the active part in mutagenesis of [6]-gingerol, a mutagen contained in ginger Zingiber officinale (Nakamura and Yamamoto, 1982). [6]-Shogaol was isolated from the ginger by column chromatography on silica gel. [6]-Shogaol was much less mutagenic (1 X 10(3) revertants/10(8) viable cells/700 microM) than [6]-gingerol (1 X 10(7) of the same units). Mutation frequencies of their related compounds were 4 X 10(1) for zingerone, 1 X 10(7) for 3-hydroxymyristic acid and 3 X 10(2) for 12-hydroxystearic acid. Curcumin, and myristic, stearic and oleic acids had no mutagenicity; and diacetone alcohol and butyroin were suppressible for mutation. It was inferred from these results that the active part of [6]-gingerol was the aliphatic chain moiety containing a hydroxy group.

Catechols↗

PubMed1990

Analysis of a thread used in the Kshara Sutra treatment in the Ayurvedic medicinal system.

From a Kshara Sutra thread which is used in the therapy of fistula in the Ayurvedic medicinal system, euphol, 3,12-di-O-acetyl-8-O-benzoylingol, 3,12-di-O-acetyl-8-O-tigloylingol, curcumin, p-coumaroylferuloylmethane and di-p-courmaroylmethane were isolated and characterized. In addition, GLC and GC/MS confirmed the presence of euphol, antiquol B, cycloeucalenol and 24-methylene cycloartanol in the thread.

Catechols↗

PubMed2005

Elevated expression of alphaA- and alphaB-crystallins in streptozotocin-induced diabetic rat.

alpha-Crystallin, a predominant protein of the ocular lens, is composed of two subunits, alphaA and alphaB. Of these, alphaB-crystallin has been shown to present widely in non-lenticular tissues while alphaA-crystallin is largely lens-specific. Although, expression of alphaB-crystallin is elevated under various stress and pathological conditions, yet its physiological significance remained unknown. Some studies suggest that the expression of alphaB-crystallin gene is related to oxidative stress. Persistent hyperglycemia during uncontrolled diabetes is known to cause oxidative stress, which has been implicated in various secondary complications of diabetes. Hence, expression of alphaA- and alphaB-crystallins in various tissues of streptozotocin (STZ)-induced diabetic Wistar-NIN rats was investigated by RT-PCR and immunoblotting. While expression of alphaB-crystallin was noted in the wide range of tissues examined in the study, alphaA-crystallin expression was detected only in lens and retina. Interestingly, alphaB-crystallin expression was elevated in lens, heart, muscle, and brain, but decreased in adipose tissue of diabetic rats compared to control rats. alphaA-Crystallin expression was increased in retina of diabetic rat. Increased oxidative stress appears to be a major stimulus for the enhanced expression of alphaA- and alphaB-crystallins in the tissues of diabetic rats and elevated expression of alpha-crystallin may have a protective role against metabolic stress. Interestingly, feeding of curcumin, a dietary antioxidant, to diabetic rats attenuated the enhanced expression of alphaB-crystallin. The results indicate that elevated expression of alpha-crystallins in some tissues may have implications in pathophysiology of diabetic complications.

Animals↗

PubMed2005

Effect of artemisinin/artesunate as inhibitors of hepatitis B virus production in an "in vitro" replicative system.

The antiviral effect against hepatitis B virus (HBV) of artemisinin, its derivative artesunate and other compounds highly purified from traditional Chinese medicine remedies, were investigated. HBV production by permanently transfected HepG2 2.2.15 cells was determined by measuring the release of surface protein (HBsAg) and HBV-DNA after drug exposure (0.01-100 microM) for 21 days. The forms of HBV-DNA released were investigated by Southern-blotting. Neutral Red retention test was used to evaluate drug-induced toxicity on host cells. The compounds were classified according to their potential interest as follows: (i) none: they had no effect on viral production (daidzein, daidzin, isonardosinon, nardofuran, nardosinon, tetrahydronardosinon and quercetin); (ii) low: they were able to markedly reduce viral production, but also induced toxicity on host cells (berberine and tannic acid) or they had no toxic effect on host cells but only had a moderate ability to reduce viral production (curcumin, baicalein, baicalin, bufalin, diallyl disulphide, glycyrrhizic acid and puerarin); (iii) high: they induced strong inhibition of viral production at concentrations at which host cell viability was not affected (artemisinin and artesunate). Moreover, artesunate in conjunction with lamivudine had synergic anti-HBV effects, which warrants further evaluation of artemisinin/artesunate as antiviral agents against HBV infection.

Anti-HIV Agents↗

PubMed2003

Involvement of multidrug resistance-associated proteins in regulating cellular levels of (-)-epigallocatechin-3-gallate and its methyl metabolites.

(-)-Epigallocatechin-3-gallate (EGCG), a major polyphenol of green tea, has many interesting biological activities. The uptake of EGCG and involvement of specific efflux pumps were studied in MDCKII cells transfected with hPgp, hMRP1, and hMRP2 genes. Total cell associated [3H]EGCG increased 7-fold in the presence of the MRP inhibitors, indomethacin and probenecid, in MDCKII/MRP1 cells, compared to a 2-fold increase in wild-type cells. Intracellular levels of EGCG, 4(")-O-methyl EGCG, and 4('),4(")-di-O-methyl EGCG were increased by 13-, 11-, and 3-fold, respectively, by indomethacin in MDCKII/MRP1 cells. Accumulation of EGCG and its methyl metabolites was also increased approximately 10-fold in the presence of MK-571 in MDCKII/MRP2 cells. Co-treatment with isoflavones, curcumin and tetrahydrocurcumin, increased [3H]EGCG accumulation significantly in MDCKII/MRP1 and HT-29 cells. The results indicate that EGCG and its methyl metabolites are substrates for MRP1 and MRP2, but not for Pgp. MRP type efflux pumps may limit the bioavailability of EGCG.

Animals↗

PubMed2004

AP-1-independent sensitization to oxidative stress-induced apoptosis by proteasome inhibitors.

Hydrogen peroxide (H(2)O(2)) induces apoptosis of mesangial cells via c-Jun N-terminal kinase (JNK)-activator protein-1 (AP-1) and extracellular signal-regulated kinase (ERK)-AP-1 pathways. We recently found that subtoxic doses of proteasome inhibitors, MG132 and lactacystin, dramatically enhanced H(2)O(2)-induced apoptosis in mesangial cells. In this report, we examined molecular mechanisms involved in this phenomenon, especially focusing on AP-1 pathways. Reporter assays showed that MG132 induced activation of AP-1. However, pharmacological inhibitors of AP-1, retinoic acid, and curcumin, did not suppress the proapoptotic effect of MG132. Suppression of JNK-AP-1 by transfection with either a dominant-negative mutant of JNK or a dominant-negative mutant of c-Jun did not attenuate the apoptosis enhancement by MG132. Similarly, suppression of ERK-AP-1 by PD98059 or dominant-negative mutants of ERK did not affect the apoptosis-promoting effect of MG132. Interestingly, pretreatment with MG132 did not enhance activation of AP-1 by H(2)O(2). These data suggested a novel, AP-1-independent promotion of apoptosis by proteasome inhibitors.

Animals↗

PubMed2005

Ferulic acid destabilizes preformed beta-amyloid fibrils in vitro.

Inhibition of the formation of beta-amyloid fibrils (fAbeta), as well as the destabilization of preformed fAbeta in the CNS, would be attractive therapeutic targets for the treatment of Alzheimer's disease (AD). We reported previously that curcumin (Cur) inhibits fAbeta formation from Abeta and destabilizes preformed fAbeta in vitro. Using fluorescence spectroscopic analysis with thioflavin T and electron microscopic studies, we examined the effects of ferulic acid (FA) on the formation, extension, and destabilization of fAbeta at pH 7.5 at 37 degrees C in vitro. We next compared the anti-amyloidogenic activities of FA with Cur, rifampicin, and tetracycline. Ferulic acid dose-dependently inhibited fAbeta formation from amyloid beta-peptide, as well as their extension. Moreover, it destabilized preformed fAbetas. The overall activity of the molecules examined was in the order of: Cur > FA > rifampicin = tetracycline. FA could be a key molecule for the development of therapeutics for AD.

Amyloid↗

PubMed2004

Increase by FK960, a novel cognitive enhancer, in glial cell line-derived neurotrophic factor production in cultured rat astrocytes.

We examined the effect of N-(4-acetyl-1-piperazinyl)-p-fluorobenzamide monohydrate (FK960), a novel anti-dementia drug, on neurotrophic factor production in cultured rat astrocytes. FK960 (100nM) increased mRNA and protein levels of glial cell line-derived neurotrophic factor (GDNF). FK960 did not affect mRNA levels of neurotrophic factors other than GDNF. The effect of FK960 was not affected by antagonists of dopamine and alpha7-nicotinic acetylcholine receptors. FK960 stimulated phosphorylation of mitogen-activated protein/extracellular signal-regulated kinase (ERK) without any effect on phosphoryolation of p38 and c-Jun N-terminal kinase. FK960 increased the levels of c-Fos and phosphorylation of cAMP responsive element binding protein (CREB). The effect of FK960 on c-Fos was inhibited by PD98059 (10microM), an ERK kinase inhibitor, and cycloheximide (1microg/ml), a transcription inhibitor, and the effect of FK960 on CREB phosphorylation was blocked by PD98059. The effect of FK960 on GDNF mRNA expression was attenuated by PD98059, curcumin (10microM), an activator protein-1 inhibitor, cycloheximide and actinomycin D (10microg/ml). These results suggest that FK960 stimulates GDNF production in c-Fos- and CREB-dependent mechanisms in cultured astrocytes and that ERK signal is responsible for both c-Fos expression and CREB phosphorylation in the cascades.

Animals↗

PubMed2004

Redox modulation of chromatin remodeling: impact on histone acetylation and deacetylation, NF-kappaB and pro-inflammatory gene expression.

Reactive oxygen species (ROS), either directly or via the formation of lipid peroxidation products, such as 4-hydroxy-2-nonenal, acrolein and F2-isoprostanes, may play a role in enhancing inflammation through the activation and phosphorylation of stress kinases (JNK, ERK, p38) and redox-sensitive transcription factors such as NF-kappaB and AP-1. This increases the expression of genes regulating a battery of distinct pro-inflammatory mediators. Acetylation by histone acetyltransferase (HAT) of specific lysine residues on the N-terminal tail of core histones, results in uncoiling of the DNA and increased accessibility to transcription factor binding. In contrast, histone deacetylation by histone deacetylase (HDAC) represses gene transcription by promoting DNA winding thereby limiting access to transcription factors. Oxidative stress activates NF-kappaB resulting in expression of pro-inflammatory mediators through the activation of intrinsic HAT activity on co-activator molecules. In addition, oxidative stress also inhibits HDAC activity and in doing so enhances inflammatory gene expression which leads to a chronic inflammatory response. Oxidative stress can also increase complex formation between the co-activator CBP/p300 and the p65 subunit of NF-kappaB suggesting a further role of oxidative stress in chromatin remodeling. The antioxidant and/or anti-inflammatory effects of thiol molecules (glutathione, N-acetyl-L-cysteine and N-acystelyn), dietary polyphenols (curcumin-diferuloylmethane and resveratrol), the bronchodilator theophylline and glucocorticoids have all been shown to play a role in either controlling NF-kappaB activation or chromatin remodeling through modulation of HDAC activity and subsequently inflammatory gene expression in lung epithelial cells. Thus, oxidative stress regulates both signal transduction and chromatin remodeling which in turn impacts on pro-inflammatory responses in the lungs.

Acetylation↗

PubMed2006

The effects of cannabinoids on P-glycoprotein transport and expression in multidrug resistant cells.

Cannabis is the most widely used illicit drug in the world. Cannabinoids are used therapeutically by some patients as they have analgesic, anti-emetic and appetite stimulant properties which palliate adverse symptoms. Use of these agents in an oncology setting raises the question of whether they act to modulate the effectiveness of concurrently administered anti-cancer drugs. The transporter, P-glycoprotein (P-gp) confers multiple drug resistance (MDR) by effluxing a diverse array of anti-cancer agents. This study was undertaken to examine the effect of cannabinoids on P-gp. Unlike the known P-gp inhibitor, PSC833, short 1h exposure to three plant-derived cannabinoids, cannabinol (CBN), cannabidiol (CBD) and Delta(9)-tetrahydrocannabinol (THC) and the synthetic cannabinoid receptor agonist, WIN55, 212-2 (WIN) did not inhibit the efflux of the P-gp substrate Rhodamine 123 (Rh123) in either a drug-selected human T lymphoblastoid leukaemia cell line (CEM/VLB(100)) or in a mouse fibroblast MDR1 transfected cell line (77.1). However, in CEM/VLB(100) cells, prolonged 72 h exposure to the cannabinoids, THC and CBD, decreased P-gp expression to a similar extent as the flavonoid, curcumin (turmeric). This correlated with an increase in intracellular accumulation of Rh123 and enhanced sensitivity of the cells to the cytotoxic actions of the P-gp substrate, vinblastine. Taken together, these results provide preliminary evidence that cannabinoids do not exacerbate P-gp mediated MDR. Further, plant-derived cannabinoids are moderately effective in reversing MDR in CEM/VLB(100) cells by decreasing P-gp expression.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2006

Regulation of inflammation and redox signaling by dietary polyphenols.

Reactive oxygen species (ROS) play a key role in enhancing the inflammation through the activation of NF-kappaB and AP-1 transcription factors, and nuclear histone acetylation and deacetylation in various inflammatory diseases. Such undesired effects of oxidative stress have been found to be controlled by the antioxidant and/or anti-inflammatory effects of dietary polyphenols such as curcumin (diferuloylmethane, a principal component of turmeric) and resveratrol (a flavonoid found in red wine). The phenolic compounds in fruits, vegetables, tea and wine are mostly derivatives, and/or isomers of flavones, isoflavones, flavonols, catechins, tocopherols, and phenolic acids. Polyphenols modulate important cellular signaling processes such as cellular growth, differentiation and host of other cellular features. In addition, they modulate NF-kappaB activation, chromatin structure, glutathione biosynthesis, nuclear redox factor (Nrf2) activation, scavenge effect of ROS directly or via glutathione peroxidase activity and as a consequence regulate inflammatory genes in macrophages and lung epithelial cells. However, recent data suggest that dietary polyphenols can work as modifiers of signal transduction pathways to elicit their beneficial effects. The effects of polyphenols however, have been reported to be more pronounced in vitro using high concentrations which are not physiological in vivo. This commentary discusses the recent data on dietary polyphenols in the control of signaling and inflammation particularly during oxidative stress, their metabolism and bioavailability.

Animals↗

PubMed2006

Role of activator protein-1 on the effect of arginine-glycine-aspartic acid containing peptides on transforming growth factor-beta1 promoter activity.

While arginine-glycine-aspartic acid-based peptidomimetics have been employed for the treatment of cardiovascular disorders and cancer, their use in other contexts remains to be explored. Arginine-glycine-aspartic acid-serine induces Transforming growth factor-beta1 transcription in human mesangial cells, but the molecular mechanisms involved have not been studied extensively. We explored whether this effect could be due to Activator protein-1 activation and studied the potential pathways involved. Addition of arginine-glycine-aspartic acid-serine promoted Activator protein-1 binding to its cognate sequence within the Transforming growth factor-beta1 promoter as well as c-jun and c-fos protein abundance. Moreover, this effect was suppressed by curcumin, a c-Jun N terminal kinase inhibitor, and was absent when the Activator protein-1 cis-regulatory element was deleted. Activator protein-1 binding was dependent on the activity of integrin linked kinase, as transfection with a dominant negative mutant suppressed both Activator protein-1 binding and c-jun and c-fos protein increment. Integrin linked kinase was, in turn, dependent on Phosphoinositol-3 kinase activity. Arginine-glycine-aspartic acid-serine stimulated Phosphoinositol-3 kinase activity, and Transforming growth factor-beta1 promoter activation was abrogated by the use of Phosphoinositol-3 kinase specific inhibitors. In summary, we propose that arginine-glycine-aspartic acid-serine activates Integrin linked kinase via the Phosphoinositol-3 kinase pathway and this leads to activation of c-jun and c-fos and increased Activator protein-1 binding and Transforming growth factor-beta1 promoter activity. These data may contribute to understand the molecular mechanisms involved in the cellular actions of arginine-glycine-aspartic acid-related peptides and enhance their relevance as these products evolve into clinical therapeutic use.

Cardiovascular Diseases↗

PubMed2005

Preparation and anti-inflammatory activities of diarylheptanoid and diarylheptylamine analogs.

Seven diarylheptylamine (12a-g) and four diarylheptanoid analogs (3-5, 9), structurally related to the natural anti-inflammatory agent oregonin (1), have been prepared from curcumin (2) for evaluation of their activity against the expression of iNOS and COX-2. Diarylheptylamine 12b and diarylheptanoid analogs can inhibit iNOS and COX-2 responses of LPS, although less potently than 1. These compounds, however, possess stronger potency than 1 against COX-2-derived PGE2 formation, of which hexahydrocurcumin (4) is the most potent one with an IC50 value of 0.7 microM.

Amines↗