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PubMed2006

Curcumin attenuates thermal hyperalgesia in a diabetic mouse model of neuropathic pain.

Diabetic neuropathic pain, an important microvascular complication in diabetes mellitus is recognised as one of the most difficult types of pain to treat. A lack of the understanding of its aetiology, inadequate relief, development of tolerance and potential toxicity of classical antinociceptives warrant the investigation of the newer agents to relieve this pain. The aim of the present study was to explore the antinociceptive effect of curcumin and its effect on tumour necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) release in streptozotocin induced diabetic mice. Four weeks after a single intraperitoneal injection of streptozotocin (200 mg/kg), mice were tested in the tail immersion and hot-plate assays. Diabetic mice exhibited significant hyperalgesia along with increased plasma glucose and decreased body weights as compared with control mice. Chronic treatment with curcumin (15, 30 and 60 mg/kg body weight; p.o.) for 4 weeks starting from the 4th week of streptozotocin injection significantly attenuated thermal hyperalgesia and the hot-plate latencies. Curcumin also inhibited the TNF-alpha and NO release in a dose dependent manner. These results indicate an antinociceptive activity of curcumin possibly through its inhibitory action on NO and TNF-alpha release and point towards its potential to attenuate diabetic neuropathic pain.

Analgesics↗

PubMed2006

The inhibition of human glutathione S-transferases activity by plant polyphenolic compounds ellagic acid and curcumin.

Glutathione S-transferases (GSTs) are multifunctional detoxification proteins that protect the cell from electrophilic compounds. Overexpression of GSTs in cancer results in resistance to chemotherapeutic agents and inhibition of the over expressed GST has been suggested as an approach to combat GST-induced resistance. The inhibition of human recombinant GSTs by natural plant products was investigated in this study. Using 1-chloro-2,4 dinitrobenzene (CDNB) as a substrate, ellagic acid and curcumin were shown to inhibit GSTs A1-1, A2-2, M1-1, M2-2 and P1-1 with IC(50) values ranging from 0.04 to 5 microM whilst genistein, kaempferol and quercetin inhibited GSTs M1-1 and M2-2 only. The predominant mode of inhibition with respect to the G and H-sites were mixed inhibition and uncompetitive to a lesser extent. The K(i) (K(i)(')) values for ellagic acid and curcumin with respect to GSH and CDNB were in the range 0.04-6 microM showing the inhibitory potency of these polyphenolic compounds. Ellagic acid and curcumin also showed time- and concentration-dependent inactivation of GSTs M1-1, M2-2 and P1-1 with curcumin being a more potent inactivator than ellagic acid. These results facilitate the understanding of the interaction of human GSTs with plant polyphenolic compounds with regards to their role as chemomodulators in cases of GST-overexpression in malignancies.

Curcumin↗

PubMed2005

The inhibitory mechanism of curcumin and its derivative against beta-catenin/Tcf signaling.

We investigated the inhibitory mechanism of curcumin and its derivative (CHC007) against beta-catenin/T-cell factor (Tcf) signaling in various cancer cell lines. Curcumin is known to inhibit beta-catenin/Tcf transcriptional activity in HCT116 cells but not in SW620 cells. To clarify the inhibitory effect of curcumin against beta-catenin/Tcf signaling, we tested several cancer cell lines. In addition, in order to verify the inhibitory mechanism, we performed reporter gene assay, Western blot, immunoprecipitation, and electrophoretic mobility shift assay. Since inhibitors downregulated the transcriptional activity of beta-catenin/Tcf in HEK293 cells transiently transfected with S33Y mutant beta-catenin gene, whose product is not induced to be degraded by adenomatous polyposis coli-Axin-glycogen synthase kinase 3beta complex, we concluded that the inhibitory mechanism was related to beta-catenin itself or downstream components. Western blot analysis suggested that no change in the amount of cytosolic and membranous beta-catenin in a cell occurred; however, nuclear beta-catenin and Tcf-4 proteins were markedly reduced by inhibitors and this lead to the diminished association of beta-catenin with Tcf-4 and to the reduced binding to the consensus DNA. In the present study, we demonstrate that curcumin and its derivative are excellent inhibitors of beta-catenin/Tcf signaling in all tested cancer cell lines and the reduced beta-catenin/Tcf transcriptional activity is due to the decreased nuclear beta-catenin and Tcf-4.

Base Sequence↗

PubMed2004

Curcumin inhibits NF-kappaB activation and reduces the severity of experimental steatohepatitis in mice.

BACKGROUND/AIMS: While oxidative stress is a feature of non-alcoholic steatohepatitis, the causal link between oxidative stress and inflammatory recruitment has yet to be demonstrated. We analysed the role of NF-kappaB redox-sensitive signalling pathway of inflammatory recruitment in experimental steatohepatitis. METHODS: Mice were fed the methionine and choline deficient (MCD) or the control diet, with or without curcumin, an NF-kappaB inhibitor, for up to 4 weeks. Histopathology, lipoperoxides, NF-kappaB/DNA binding and expression of NF-kappaB-regulated genes were assessed. RESULTS: MCD-fed mice developed steatohepatitis accompanied by dramatic accumulation of hepatic lipoperoxides, activation of NF-kappaB and induction of pro-inflammatory ICAM-1, COX-2, MCP-1 and CINC mRNA. Curcumin significantly reduced MCD-induced inflammation but had no effect on steatosis or on the level of hepatic lipid peroxides. Curcumin prevented the MCD-induced activation of NF-kappaB and decreased downstream induction of ICAM-1, COX-2 and MCP-1. However, it failed to reduce activation of AP-1, MAPK pathways or CINC expression. CONCLUSIONS: Curcumin alleviates the severity of hepatic inflammation in experimental steatohepatitis induced by the MCD diet, an effect likely to be mediated via inhibition of NF-kB activation and dependent pro-inflammatory genes. The NF-kappaB pathway is one among several possible signalling pathways by which inflammation is recruited in experimental steatohepatitis.

Animals↗

PubMed2005

Synthesis and characterization of dual function vanadyl, gallium and indium curcumin complexes for medicinal applications.

Novel bis[4-hydroxy-3-methoxyphenyl]-1,6-heptadiene-3,5-dione (curcumin) complexes with the formula, ML(3), where M is Ga(III) or In(III), or of the formula, ML(2) where M is [VO](2+), have been synthesized and characterized by mass spectrometry, infrared and absorption spectroscopies, and elemental analysis. A new ligand, bis[4-acetyl-3-hydroxyphenyl]-1,6-heptadiene-3,5-dione (diacetylbisdemethoxycurcumin, DABC) was similarly characterized; an X-ray structure analysis was performed. Vanadyl complexes tested in an acute i.p. testing protocol in STZ-diabetic rats showed a lack of insulin enhancing potential. Vanadyl complexes were, however, more cytotoxic than were the ligands alone in standard MTT (3-[4,5-dimethylthiazole-2-yl]ate, -2,5-diphenyl-tetrazolium bromide) cytotoxicity testing, using mouse lymphoma cells. With the exception of DABC, that was not different from VO(DABC)(2), the complexes were not significantly different from one another, with IC(50) values in the 5-10 microM range. Gallium and indium curcumin complexes had IC(50) values in the same 5-10 microM range; whereas Ga(DAC)(3) and In(DAC)(3) (where DAC=diacetylcurcumin) were much less cytotoxic (IC(50)=20-30 microM). Antioxidant capacity was decreased in VO(DAC)(2), Ga(DAC)(3), and In(DAC)(3), compared to vanadyl, gallium and indium curcumin, corroborating the importance of curcumin's free phenolic OH groups for scavenging oxidants, and correlated with reduced cytotoxic potential.

Animals↗

PubMed2005

Stability-indicating HPTLC determination of curcumin in bulk drug and pharmaceutical formulations.

A simple, selective, precise and stability-indicating high-performance thin-layer chromatographic method of analysis of curcumin both as a bulk drug and in formulations was developed and validated. The method employed TLC aluminium plates precoated with silica gel 60 F-254 as the stationary phase. The solvent system consisted of chloroform:methanol (9.25:0.75 v/v). This system was found to give compact spots for curcumin (R(f) value of 0.48 +/- 0.02). Densitometric analysis of curcumin was carried out in the absorbance mode at 430 nm. The linear regression analysis data for the calibration plots showed good linear relationship with r = 0.996 and 0.994 with respect to peak height and peak area, respectively, in the concentration range 50-300 ng per spot. The mean value +/- S.D. of slope and intercept were 1.08 +/- 0.01, 51.93 +/- 0.54 and 8.39 +/- 0.21, 311.55 +/ -3.23 with respect to peak height and area, respectively. The method was validated for precision, recovery and robustness. The limits of detection and quantitation were 8 and 25 ng per spot, respectively. Curcumin was subjected to acid and alkali hydrolysis, oxidation and photodegradation. The drug undergoes degradation under acidic, basic, light and oxidation conditions. This indicates that the drug is susceptible to acid, base hydrolysis, oxidation and photo oxidation. Statistical analysis proves that the method is repeatable, selective and accurate for the estimation of said drug. As the method could effectively separate the drug from its degradation product, it can be employed as a stability-indicating one.

Calibration↗

PubMed2004

Role of curcumin, a naturally occurring phenolic compound of turmeric in accelerating the repair of excision wound, in mice whole-body exposed to various doses of gamma-radiation.

The healing of irradiated wounds has always been a central consideration in medical practice because radiation disrupts normal response to injury, leading to a protracted recovery period. The quest for clinically effective wound healing agents is important in the medical management of irradiated wounds. Therefore, the present study was conceptualized to investigate the effect of curcumin (natural yellow, diferuloylmethane), a major yellow pigment and an active component of turmeric on wound healing in mice exposed to whole-body gamma-radiation. A full-thickness wound was created on the dorsum of mice whole-body irradiated to 2, 4, 6, or 8 Gy. The progression of wound contraction was monitored periodically by capturing video images of the wound. The collagen, hexosamine, DNA, nitric oxide, and histological profiles were evaluated at various postirradiation days in mice treated and not treated with curcumin before exposure to 0 or 6 Gy. The whole-body exposure resulted in a dose-dependent delay in wound contraction and prolongation of wound healing time. Irradiation caused a significant reduction in collagen, hexosamine, DNA, and nitric oxide synthesis. Pretreatment with curcumin significantly enhanced the rate of wound contraction, decreased mean wound healing time, increased synthesis of collagen, hexosamine, DNA, and nitric oxide and improved fibroblast and vascular densities. This study demonstrates that curcumin pretreatment has a conducive effect on the irradiated wound and could be a substantial therapeutic strategy in initiating and supporting the cascade of tissue repair processes in irradiated wounds.

Animals↗

PubMed2003

Changes in temperature modulate heme oxygenase-1 induction by curcumin in renal epithelial cells.

The stress protein heme oxygenase-1 (HO-1) plays an essential role in the prevention of transplant-associated organ injury and rejection. Prior to transplantation, organs are normally subjected to variable periods of cold storage in appropriate preservation solutions. Here, we examined whether curcumin, a phenolic plant extract which strongly induces HO-1 in many cell types, could up-regulate HO-1 protein in cultured renal epithelial cells at temperatures lower than the physiological 37 degrees C. We found that stimulation of HO-1 following incubation of cells with curcumin for 6h was dramatically reduced by decreasing the temperature from 37 to 10 degrees C. Interestingly, renal cells displayed high HO-1 expression and heme oxygenase activity when exposed to a programmed change in temperature that consisted of 3h at 37 degrees C followed by 1.5h at 20 degrees C and 1.5h at 10 degrees C. Increased HO-1 levels were observed also after incubation of cells with curcumin during the programmed change in temperature under hypoxia, another feature typical of cold storage procedures. Upon challenge with an oxidant-generating system, cells pretreated with curcumin at 37 degrees C or during the programmed change in temperature exhibited increased resistance to oxidative stress-mediated injury. These findings highlight the feasibility of modulating HO-1 expression during hypothermic storage to confer tissues a better protection to counteract the damage characteristic of organ transplantation.

Animals↗

PubMed2000

Differential modulation of nitric oxide production by curcumin in host macrophages and NK cells.

Curcumin, the yellow pigment from Curcuma longa, has been shown to possess tumoricidal activity. We have earlier reported the induction of apoptosis in AK-5, rat histiocytic cells by curcumin leading to the inhibition of tumor growth in vivo. In this study we have observed differential activation status in host macrophages and NK cells induced by curcumin during the spontaneous regression of subcutaneously transplanted AK-5 tumors. Closer scrutiny of the cytokine profile and nitric oxide (NO) production by immune cells showed an initial downregulation of Th1 cytokine response and NO production by macrophages, and their upregulation in NK cells, which picked-up upon prolonged treatment with curcumin, culminating in a stronger tumoricidal effect. These studies suggest that the host macrophages and NK cells play an important modulatory role in the remission of AK-5 tumor.

Animals↗

PubMed2002

Curcumin induces apoptosis in human breast cancer cells through p53-dependent Bax induction.

The aim of this study was to determine the mechanisms of curcumin-induced human breast cancer cell apoptosis. From quantitative image analysis data showing an increase in the percentage of cells with a sub-G0/G1 DNA content, we demonstrated curcumin-induced apoptosis in the breast cancer cell line MCF-7, in which expression of wild-type p53 could be induced. Apoptosis was accompanied by an increase in p53 level as well as its DNA-binding activity followed by Bax expression at the protein level. Further experiments using p53-null MDAH041 cell as well as low and high p53-expressing TR9-7 cell, in which p53 expression is under tight control of tetracycline, established that curcumin induced apoptosis in tumor cells via a p53-dependent pathway in which Bax is the downstream effector of p53. This property of curcumin suggests that this molecule could have a possible therapeutic potential in breast cancer patients.

Antineoplastic Agents, Phytogenic↗

PubMed2003

Human colon cancer cells differ in their sensitivity to curcumin-induced apoptosis and heat shock protects them by inhibiting the release of apoptosis-inducing factor and caspases.

Mild heat treatment induced the expression of heat shock protein-70 (hsp70), hsp90 and hsp27 in two human colon cancer cell lines, one derived from primary tumor, SW480, and the other derived from the secondary lymph node tissue, SW620, of the same patient. SW620 cells appear to be more sensitive to curcumin-induced apoptosis. Heat shock protects both the human colon cancer cells from curcumin-induced apoptosis. Heat shock prevented, at least in part, the release of apoptosis inducing factor from mitochondria induced by curcumin although the release of second mitochondria derived activator of caspase and cytochrome c was unaffected in both the cells. Moreover, heat shock reduced curcumin-induced activation of caspases 9 and 3 but not 8.

Apoptosis↗

PubMed2003

Production of unnatural glucosides of curcumin with drastically enhanced water solubility by cell suspension cultures of Catharanthus roseus.

Catharanthus roseus cell suspension cultures converted exogenously supplied curcumin to a series of glucosides, none of which has been found in nature so far. The efficiency of glucosylation was dependent on culture stage of the cells and medium sucrose concentration. Methyl jasmonate and salicylic acid enhanced the glucoside formation only when they were added to the cultures prior to the addition of curcumin. The glucoside yield was 2.5 micromol/g fresh weight of the cells at an optimal culture condition. The water solubility of curcumin-4',4"-O-beta-D-digentiobioside was 0.65 mmol/ml, which was 20 million-fold higher than that of curcumin.

Acetates↗

PubMed1997

Inhibitory effect on curcumin on mammalian phospholipase D activity.

Curcumin, the major yellow pigment of turmeric (Curcuma longa), has strong anti-carcinogenic and anti-inflammatory activities. We examined the effects of curcumin on enzyme activities of the following phospholipases in a cell-free system: G protein-mediated phospholipase D (PLD), phosphatidylinositol-specific phospholipase C, and phospholipase A2 from mouse macrophage-like cell line J774.1 cells, sphingomyelinase from bovine brain, and phosphatidylcholine-phospholipase C from Bacillus cereus. Curcumin inhibited several types of phospholipases, most effectively PLD among those tested. It also inhibited 12-O-tetradecanoylphorbol-13-acetate-induced PLD activation in intact J774.1 cells in a dose-dependent manner. These results suggest that the anti-inflammatory and anti-carcinogenic action of curcumin is partly due to the inhibition of PLD.

Animals↗

PubMed2001

Protection of radiation-induced protein damage by curcumin.

Free radical reactions of lysozyme (Lz), tryptophan and disulfides were studied with curcumin, a lipid-soluble antioxidant from turmeric, in aqueous solution using a pulse radiolysis technique. The binding of curcumin with lysozyme was confirmed using absorption, fluorescence and stopped-flow techniques. The free radicals of curcumin generated after repairing radicals of disulfides, lysozyme and tryptophan absorb at 500-510 nm. Implication of this in evaluating the antioxidant behavior of curcumin in protecting proteins is discussed.

Algorithms↗

PubMed2002

Curcumin inhibits telomerase activity through human telomerase reverse transcritpase in MCF-7 breast cancer cell line.

The inhibitory effect of curcumin, the yellow-colored pigment from turmeric, on telomerase activity was analyzed in human mammary epithelial (MCF-10A) and breast cancer (MCF-7) cells. Telomerase activity in MCF-7 cells is 6.9-fold higher than that of human mammary epithelial cells. In MCF-7 cells, telomerase activity decreased with increasing concentrations of curcumin, inhibiting about 93.4% activity at 100 microM concentration. The inhibition of telomerase activity in MCF-7 cells may be due to down-regulation of hTERT expression. Increasing concentrations of curcumin caused a steady decrease in the level of hTERT mRNA in MCF-7 cells whereas the level of hTER and c-myc mRNAs remained the same. Our results suggest that curcumin inhibits telomerase activity by down-regulating hTERT expression in breast cancer cells and this down-regulation is not through the c-myc pathway.

Breast Neoplasms↗

PubMed1998

Strand scission in DNA induced by curcumin in the presence of Cu(II).

Curcumin, a naturally occurring phytochemical responsible for the colour of turmeric, has shown a wide range of pharmacological properties including anti-inflammatory, anti-tumour promoter and anti-oxidant effects. In this paper we show that in the presence of Cu(II), curcumin caused breakage of calf thymus and supercoiled plasmid pBR322 DNA. The products were relaxed circles with no detectable linear forms. Other metal ions tested (Mg(II), Ca(II), Fe(II) and Ni(II)) were ineffective or less effective in the DNA breakage reaction. Cu(I) was shown to be an essential intermediate by using the Cu(I)-specific sequestering reagent neocuproine. The involvement of active oxygen species, such as H2O2 and (1)O2 was established by the inhibition of DNA breakage by catalase and azide. Curcumin is also able to directly produce O2- and H2O2 and in the presence of Cu(II), OH is generated. Absorption spectra of curcumin in the presence of DNA indicated that a complex is formed between the two. The results are discussed in relation to the established pro-oxidant activities of other known anti-oxidants.

Animals↗

PubMed2000

Dietary curcumin prevents ocular toxicity of naphthalene in rats.

Administration of naphthalene is known to cause cataract formation in rats and rabbits and naphthalene-initiated cataract is frequently used as a model for studies on senile cataract in humans. Oxidative stress has been implicated in the mechanism of naphthalene-induced cataract. Curcumin, a constituent of turmeric, a spice used in Indian curry dishes, is an effective antioxidant and is known to induce the enzymes of glutathione-linked detoxification pathways in rats. During the present studies, we have examined whether low levels of dietary curcumin could prevent naphthalene-induced opacification of rat lens. The presence of apoptotic cells in lens epithelial cells was also examined by catalytically incorporating labeled nucleotide to DNA with either Klenow fragment of DNA polymerase or by terminal deoxynucleotidyl transferase (TdT), which forms polymeric tail using the principle of TUNEL assay. The results of these studies demonstrated that the rats treated with naphthalene and kept on a diet supplemented with only 0.005% (w/w) curcumin had significantly less opacification of lenses as compared to that observed in rats treated only with naphthalene. Our studies also demonstrate, for the first time, that naphthalene-initiated cataract in lens is accompanied and perhaps preceded by apoptosis of lens epithelial cells and that curcumin attenuates this apoptotic effect of naphthalene.

Administration, Oral↗

PubMed2002

Studies of curcumin and curcuminoids. XXVII. Cyclodextrin complexation: solubility, chemical and photochemical stability.

Cyclodextrin complexes of the natural compound curcumin were prepared in order to improve the water solubility and the hydrolytic and photochemical stability of the compound. Complex formation resulted in an increase in water solubility at pH 5 by a factor of at least 10(4). The hydrolytic stability of curcumin under alkaline conditions was strongly improved by complex formation, while the photodecomposition rate was increased compared to a curcumin solution in organic solvents. The cavity size and the charge and bulkiness of the cyclodextrin side-chains influenced the stability constant for complexation and the degradation rate of the curcumin molecule.

Chromatography, High Pressure Liquid↗