Showing papers on "Curcumin published in 1996"
TL;DR: The antioxidants, N-acetyl-L-cysteine (NAC), L-ascorbic acid, alpha-tocopherol, catalase and superoxide dismutase, all effectively prevented curcumin-induced apoptosis, suggesting that curcuming-induced cell death was mediated by reactive oxygen species.
413 citations
TL;DR: It is suggested that THC may also exhibit the same physiological and pharmacological properties as the active form of curcumin in vivo by means of the beta-diketone moiety as well as phenolic hydroxy groups.
392 citations
TL;DR: While curcumin was highly effective as a chemopreventive agent in the colon model, it was only weakly effective in the mammary model and quercetin caused a dose-dependent enhancement of tumors induced by AOM in the Colon model.
Abstract: Curcumin and quercetin were evaluated in rats for their ability to modulate the carcinogenic activity of azoxymethane (AOM) in the colon and 7,12-dimethylbenz[a]anthracene (DMBA) in the mammary gland. In the AOM-induced colon cancer model, male Fischer 344 rats at 8 weeks of age started to receive either curcumin (8 and 16 g/kg) or quercetin (16.8 and 33.6 g/kg) in the diet and 1 week later, were administered AOM (30 mg/kg body wt.) by subcutaneous injection. The animals continued to receive the two agents in the diet until sacrificed 45 weeks later. Curcumin mediated a dose-dependent inhibition of the incidence and multiplicity of adenomas from 47% and 0.58 +/- 0.12 adenomas/rat in the AOM-treated control group to 19% and 0.22 +/- 0.08 and 0.06% and 0.08 +/- 0.06 adenomas/rat for the low and high dose groups, respectively. A low yield of adenocarcinomas (0.06 +/- 0.04 adenocarcinomas/rat) was induced by AOM which was not significantly altered by curcumin. Treatment with quercetin caused a dose-dependent increase in the yield of AOM-induced tumors in the colon from 0.06 +/- 0.04 adenocarcinoma/rat to 0.64 +/- 0.12 and 1.14 +/- 0.17 for the low and high dose groups, respectively. In the DMBA-induced mammary cancer model, curcumin or quercetin was administered at either 10 or 20 g/kg diet, beginning 7 days prior to DMBA and continually throughout the remainder of the experiment. Neither curcumin nor quercetin significantly altered the incidence of animals with tumors or the tumor multiplicity, while the high concentration of both agents significantly increased tumor latency. These results demonstrate different responses to these agents in the two models. While curcumin was highly effective as a chemopreventive agent in the colon model, it was only weakly effective in the mammary model. In contrast, quercetin which was also only weakly effective in the mammary model, caused a dose-dependent enhancement of tumors induced by AOM in the colon model.
260 citations
TL;DR: These strong inhibitory properties of curcumin towards P450s and GSTs, in addition to its well-known antioxidant activity, may help explain the previously observed anticarcinogenic, antimutagenic, and cytoprotective effects of this important natural compound and food constituent.
258 citations
TL;DR: Curcumin could have a protective effect against the damage caused by myocardial infarction and was shown to have a membrane stabilizing action by inhibiting the release of β-glucuronidase from nuclei, mitochondria, lysosome and microsome.
Abstract: The effect of curcumin on the biochemical changes induced by isoproterenol (ISO) administration in rats was examined. ISO (300 mg Kg−1 administered subcutaneously twice at an interval of 24 h) caused a decrease in body weight and an increase in heart weight, water content as well as in the levels of serum marker enzymes viz creatine kinase (CK), lactate dehydrogenase (LDH) and LDH1 isozyme. It also produced electrocardiographic changes such as increased heart rate, reduced R amplitude and ST elevation. Curcumin at a concentration of 200 mg.Kg−1 when administered orally, showed a decrease in serum enzyme levels and the electrocardiographic changes got restored towards normalcy. Myocardial infarction was accompanied by the disintegration of membrane polyunsaturated fatty acids expressed by increase of thiobarbituric acid reactive substance (TBARS), a measure of lipid peroxides and by the impairment of natural scavenging, characterized by the decrease in the levels of superoxide dismutase, catalase, glutathione peroxidase, ceruloplasmin, alpha tocopherol, reduced glutathione (GSH) and ascorbic acid. The oral pretreatment with curcumin two days before and during ISO administration decreased the effect of lipid peroxidation. It was shown to have a membrane stabilizing action by inhibiting the release of β-glucuronidase from nuclei, mitochondria, lysosome and microsome. Curcumin pre- and co-treatment decreased the severity of pathological changes and thus, could have a protective effect against the damage caused by myocardial infarction (MI).
232 citations
TL;DR: Curcumin may be an effective protective agent against cataractogenesis induced by lipid peroxidation in an in vitro rat model and the lenses from curcumin-treated rats were much more resistant to 4-HNE-induced opacification than were lenses from control animals.
143 citations
TL;DR: Salicylcurcuminoid, which was causing no papillomas by the 10th week of tumour initiation, was the most potent anti-carcinogen among the synthetic curcuminoids and Piperonal cur cuminoid also exhibited anti-promotional activity.
Abstract: Five synthetic curcuminoids and three natural curcuminoids were investigated for their antimutagenic and anti-promotional activity. The natural curcuminoids, curcumin I (diferuloylmethane), curcumin II (feruloyl- p -hydroxycin-namoylmethane) and curcumin III (bis-( p -hydroxycinnamoyl)methane) isolated from Curcuma longa were found to be potent inhibitors of mutagenesis and crotean oil-induced tumour promotion. Curcumin III produced 87.6% inhibition to 2-acetamidofluorene (2-AAF) induced mutagenesis, at a concentration of 100 μg/plate, curcumin II and curcumin I produced 70.5% and 68.3% inhibition at the same concentration. All the synthetic curcuminoids were found to inhibit 2-AAF-induced mutagenicity among which salicyl-and anisylcurcuminoids were the most active. Curcumin III was the most effective anti-promotor among natural curcuminoids. While 90% of the control animals were having papillomas on the 10th week of tumour initiation, only 10% of the curcumin III-treated animals, 20% of the curcumin II-treated animals, and 40% of the curcumin I-treated animals were having papillomas. Salicylcurcuminoid, which was causing no papillomas by the 10th week, was the most potent anti-carcinogen among the synthetic curcuminoids. Piperonal curcuminoid also exhibited anti-promotional activity.
135 citations
TL;DR: Reversible inhibition of GST was the major mechanism of inhibition of DNPSG-excretion in melanoma cells, except in the cases of curcumin and ethacrynic acid, which compounds also inactivated GSTP1-1 by covalent modification.
116 citations
TL;DR: A unique mode of action of curcumin is revealed whereby it effectively blocked the cell cycle progression during S-phase by inhibiting the activity of TK enzyme.
102 citations
TL;DR: Rats treated with isoproterenol showed a significant increase in serum lysosomal hydrolase activities, which were found to decrease after curcumin treatment, and Histopathological studies of the infarcted rat heart showed a decreased degree of necrosis after cur cumin treatment.
102 citations
TL;DR: Curcumin when administered i.p. can act as an effective chemopreventative agent towards DMBA-induced rat mammary tumorigenesis and mammary adduct formation.
TL;DR: Findings suggest that curcumin may induce the expression of the HSP70 gene through the initial depletion of intracellular Ca+2, followed by the suppression of p53 gene function in the target cells.
Abstract: Curcumin (diferuloyl methane) is the major active yellow pigment of turmeric and curry. Studies in recent years have indicated that curcumin is a potent inhibitor of the initiation and promotion of chemical carcinogen-induced skin carcinogenesis in mice. When COLO205 colorectal carcinoma cells were treated with curcumin (60 microM), the appearance of apoptotic DNA ladders was delayed about 5 h, and G1 arrest was detected. Further analysis of the endonuclease activities in these cells revealed that the activity of Ca(+2)-dependent endonuclease in COLO205 cells was profoundly inhibited and that the extent of inhibition depended on the degree of calcium depletion. The reduction of p53 gene expression was accompanied by the induction of HSP70 gene expression in the curcumin-treated cells. These findings suggest that curcumin may induce the expression of the HSP70 gene through the initial depletion of intracellular Ca(+2), followed by the suppression of p53 gene function in the target cells.
TL;DR: The case of curcumin was studied in this article, where it was shown that it has cytotoxicity and cytoprotective activities of natural compounds, and the case of Curcumin showed that it is a compound with good properties.
Abstract: (1996). Cytotoxicity and cytoprotective activities of natural compounds. The case of curcumin. Xenobiotica: Vol. 26, No. 7, pp. 667-680.
TL;DR: The results indicated that synthetic curcuminoids, like naturalCurcumin, are potent antioxidants.
TL;DR: Curcumin inhibits cAK, PKC and CDPK in a fashion that is competitive with respect to both ATP and the synthetic peptide substrate employed and largely overcomes inhibition of cAK by curcumin.
TL;DR: Curcumin, in a dose-dependent manner, inhibited the formation of covalent adduct between aflatoxin B1 and DNA, as catalyzed by microsomes or a reconstituted microsomal monooxygenase system, and may inhibit chemical carcinogenesis by modulating cytochrome P450 function.
Patent•
26 Sep 1996
TL;DR: In this article, a method of inhibiting the activation of the NFκB transcription factor in an animal in need of such treatment comprising the step of administering to said animal a pharmacologically effective dose of curcumin is presented.
Abstract: The present invention provides a method of inhibiting the activation of the NFκB transcription factor in an animal in need of such treatment comprising the step of administering to said animal a pharmacologically effective dose of curcumin. Also provided is a method of inhibiting the nuclear translocation of the p65 subunit of the NFκB transcription factor in a cell or in an animal in need of such treatment comprising the step of administering to said animal a pharmacologically effective dose of curcumin.
TL;DR: Modulation in competing potential pathways of biotransformation system enzymes in lactating dams may affect the rate and extent of maternal detoxication and thus influence the passage of metabolites of administered xenobiotics to the suckling neonate.
Abstract: The present study assesses the potential of arecoline alkaloid to translactationally modify the chemopreventive efficacy of curcumin (diferuloyl methane) via neonatal modulation of hepatic biotransformation system enzymes. Curcumin (0.4 g/kg body wt/day) induced a significant increase in the hepatic levels of glutathione‐S‐transferase (GST), acid‐soluble sulfhydryl (SH), cytochrome b5, and cytochrome P‐450 in lactating dams and F1 pups at 14 or 21 days. Arecoline (20 mg/kg body wt/day) could not modulate the hepatic GST and SH levels, although significant induction was observed in the levels of cytochrome b5 and cytochrome P‐450 in dams and suckling pups. Significant enhancement of hepatic GST, SH, cytochrome b5, and cytochrome P‐450 levels was observed in groups treated with curcumin + arecoline. Curcumin‐induced levels of GST and SH were depressed whereas cytochrome b5 and cytochrome P‐450 were further elevated by curcumin + arecoline treatment. The elevated levels of Phase I enzymes were more ...
01 Jan 1996
TL;DR: This study indicates that curcumin or eugenol reduces the iron-induced hepatic damage by lowering lipid peroxidation.
Abstract: Male Wistar rats injected i.p. with 30 mg Fe’+ikg body weight show hepatic damage as measured by an increase
in lipid peroxides which correlated with elevated serum enzymes, alanine aminotransferase (ALAT), aspartate amino-
transferase (ASAT) and lactate dehydrogenase (LDH). Oral administration of spice principles, curcumin from turmeric
(30 mgkg body weight) or eugenol from cloves (100 mgkg body weight), for 10 days lowered the liver and serum lipid
peroxide levels, serum ALAT, ASAT and LDH, enhanced by i.p. injection of iron. This study indicates that curcumin
or eugenol reduces the iron-induced hepatic damage by lowering lipid peroxidation.
Journal Article•
TL;DR: Evidence is provided that turmeric and curcumin provide protection against oxidative stress in a renal cell line and gave as much protection as did vitamin E in both chromium release assay and lipid degradation.
Abstract: Cell injury by oxidative stress is an important mechanism for renal epithelial cell destruction. This study observed the protective effect of turmeric and its constituents on H2O2-induced injury. Turmeric consists of a water soluble turmerin and lipid soluble curcumin with potent antioxidant properties. Confluent LLC-PK1 cells were labelled with 3H-arachidonic acid at 0.1 microCi/ml over 18 h and then further labelled with 51Cr. Turmeric ( 100 microg/ml-0.1 microg/ml), turmerin (800 ng/ml-0.8 ng/ml), curcumin (100 microg/ml-0.1 microg/ml), vitamin E (100 microM) and 21-aminosteroid (20 microM) were added and incubated for 3 h at 37 degrees C in 24-well plate. The adherent cells were washed and incubated for 3 h with 1.5 mM H2O2 at 37 degrees C. 3H-arachidonic acid release, 51Cr release and lipid peroxidation by the thiobarbituric acid reaction was determined. Turmeric ( 100 microg/ml) and curcumin (100 microg/ml, 10 microg/ml) gave as much protection as did vitamin E in both chromium release assay and lipid degradation while Turmeric (100 microg/ml) and curcumin (100 microg/ml) gave comparable inhibition of lipid peroxidation. Turmerin and 21-aminosteroid showed no protection. These findings provide evidence that turmeric and curcumin provide protection against oxidative stress in a renal cell line.
Patent•
22 Mar 1996
TL;DR: In this paper, a curcuminoid, such as Curcumin, demethoxyCurcumin or bisdemethoxycurcumin obtained from a plant of the family Zingiberaceae, was used to prevent prostate hypertrophy.
Abstract: PROBLEM TO BE SOLVED: To provide a substance having high safety and capable of being a daily ingestible preventive for prostatic hypertrophy and to provide an ingesta containing the substance. SOLUTION: A curcuminoid such as curcumin, demethoxycurcumin or bisdemethoxycurcumin obtained from a plant of the family Zingiberaceae manifests an inhibiting action for testosterone-5α-reductase. This invention claims a utilization of the curcuminoid to prevention, remedy, etc., for prostatic hypertrophy.
01 Feb 1996
TL;DR: A study by the Community Research Initiatives of New England (CRINE) shows no anti-HIV activity associated with curcumin, a popular herbal medication derived from the spice turmeric.
Abstract:
A study by the Community Research Initiatives of New England (CRINE) shows no anti-HIV activity associated with curcumin, a popular herbal medication derived from the spice turmeric. This study contrasts an earlier one done by the Search Alliance of Los Angeles, which observed a reduction in viral load. CRINE attempted to reproduce the earlier results by enrolling forty people in a study. Two dosages were used and results were nil for both dosages. Neither viral load nor CD4 counts changed significantly over eight weeks. One possible reason for curcumin's lack of activity is that it is poorly absorbed in the digestive tract.