SEARCH · PubMed Health

Results for “Curcumin”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 1,369 records · Page 76Linked to original sources

PubMed2003

Design and development of integrase inhibitors as anti-HIV agents.

A review is presented on different categories of compounds that have been studied for the inhibition of the HIV-1 integrase to develop anti-HIV agents. These compounds are: oligonucleotides (double-stranded, triplex, and G-quartet), curcumin analogues, polyhydroxylated aromatic compounds, diketo acids, caffeoyl- and galloyl - based compounds, hydrazides and amides, tetracyclines, and depsides and depsidones. For all these compounds, the important structural features essential for the inhibition of the integrase are pointed out.

Amides↗

PubMed1991

Identification of 12(S)-hydroxyeicosatetraenoic acid in the young rat lens.

Evidence is presented indicating that young rat lens has the capacity to synthesize 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE) from exogenous arachidonic acid (AA). A 9,000 xg supernatant prepared from 15 day old rat lenses, when incubated with calcium and U-[14C]-AA, generated a radiolabelled product with a retention time identical to authentic unlabelled 12-HETE in two different HPLC solvent systems. Mass spectral analysis provided evidence that the metabolite was 12-HETE while chiral studies demonstrated the exclusive presence of the 12(S) isomer. Radiolabelled 12-HETE synthesis was inhibited by preincubating the 15 day old rat lens supernatant with 0.2 Mm curcumin, a mixed cyclooxygenase/lipoxygenase inhibitor. Radiolabelled 12(S)-HETE synthetic capacity was highest in the 4 day old rat lens, the earliest time period measured, and rapidly declined with age reaching negligible levels at about 4 months. These results suggest that the young rat lens possess the biosynthetic capacity to generate radiolabelled 12(S)-HETE from U-[14]C-AA. The profile of 12-HETE synthetic activity suggests a possible regulatory function of the hydroxylated AA metabolite in the developing lens.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMedDate not supplied

Effect of cobalt ion on radical intensity and cytotoxic activity of antioxidants.

The effect of CoCl2 on the cytotoxic activity of various antioxidants against human oral tumor cell lines (HSC-2, HSG) and normal human gingival fibroblasts (HGF) was investigated. Noncytotoxic concentrations of CoCl2 significantly reduced the cytotoxic activity of sodium ascorbate, gallic acid, epigallocatechin gallate (EGCG), curcumin and dopamine, but not that of sodium 5,6-benzylidene-L-ascorbate (SBA) and benzaldehyde. Among these compounds, benzaldehyde showed the most prominent tumor-specific cytotoxic action. ESR spectroscopy showed that these antioxidants produced radicals under alkaline condition and that their radical intensity was transiently enhanced and finally disappeared by addition of CoCl2. Antioxidants which are sensitive to CoCl2 generally had higher cytotoxic activity and oxidation potential (measured by NO monitor) and addition of CoCl2 significantly reduced their oxidation potential. The present study suggests that cobalt ion stimulates the oxidation of antioxidants to their inactive products.

Antioxidants↗

PubMed2002

Amyloid-beta induces Smac release via AP-1/Bim activation in cerebral endothelial cells.

Insoluble fibrils of amyloid-beta peptide (Abeta) are the major component of senile and vascular plaques found in the brains of Alzheimer's disease (AD) patients. Abeta has been implicated in neuronal and vascular degeneration because of its toxicity to neurons and endothelial cells in vitro; some of these cells die with characteristic features of apoptosis. We used primary cultures of murine cerebral endothelial cells (CECs) to explore the mechanisms involved in Abeta-induced cell death. We report here that Abeta(25-35), a cytotoxic fragment of Abeta, induced translocation of the apoptosis regulator termed second-mitochondria-derived activator of caspase (Smac) from the intramembranous compartment of the mitochondria to the cytosol 24 hr after exposure. In addition, we demonstrated that X chromosome-linked inhibitor-of-apoptosis protein (XIAP) coimmunoprecipitated with Smac, suggesting that the two proteins bound to one another subsequent to the release of Smac from the mitochondria. Abeta(25-35) treatment also led to rapid AP-1 activation and subsequent expression of Bim, a member of the BH3-only family of proapoptotic proteins. Bim knockdown using an antisense oligonucleotide strategy suppressed Abeta(25-35)-induced Smac release and resulted in attenuation of CEC death. Furthermore, AP-1 inhibition, with curcumin or c-fos antisense oligonucleotide, reduced bim expression. These results suggest that Abeta activates an apoptotic cascade involving AP-1 DNA binding, subsequent bim induction, followed by Smac release and binding to XIAP, resulting in CEC death.

Amyloid beta-Peptides↗

PubMed2003

Rapid and selective apoptosis in human leukemic cells induced by Aplidine through a Fas/CD95- and mitochondrial-mediated mechanism.

Aplidine is a promising antitumor agent derived from the Mediterranean tunicate Aplidium albicans. We have found that Aplidine at nM concentrations (10-100 nM) induced apoptosis in human leukemic cell lines and primary leukemic cell cultures from leukemic patients. Inhibition of the Fas (CD95)/Fas ligand (CD95L) signaling pathway with an antagonistic anti-Fas antibody partially inhibited Aplidine-induced apoptosis. L929 cells were resistant to Aplidine action but underwent apoptosis after transfection with human Fas cDNA. Aplidine induced a rapid and sustained c-Jun NH(2)-terminal kinase activation, and pretreatment with curcumin or SP600125 inhibited Aplidine-induced c-Jun NH(2)-terminal kinase activation and apoptosis. However, inhibition of extracellular signal-regulated kinase and p38 kinase signaling pathways did not affect Aplidine-induced apoptosis. Aplidine induced caspase-3 activation, and caspase inhibition prevented Aplidine-induced apoptosis. Aplidine failed to induce apoptosis in MCF-7 breast cancer cells, defective in caspase-3, additionally implicating caspase-3 in its proapoptotic action. Aplidine also triggered an early release of cytochrome c from mitochondria, and overexpression of bcl-2 by gene transfer abrogated mitochondrial cytochrome c release and apoptosis. Aplidine rapidly induced cleavage of Bid, a mediator that connects the Fas/CD95 cell death receptor to the mitochondrial apoptosis pathway. Primary cultures of normal human cells, including hepatocytes and resting peripheral blood lymphocytes, were spared or weakly affected after Aplidine treatment. Nevertheless, mitogen (phytohemagglutinin/interleukin-2)-activated T lymphocytes resulted sensitively to the apoptotic action of Aplidine. Thus, Aplidine is an extremely potent and rapid apoptotic inducer on leukemic cells that triggers Fas/CD95- and mitochondrial-mediated apoptotic signaling routes, and shows a rather selective apoptotic action on cancer cells and activated T cells.

Anthracenes↗

PubMed2003

Studies on the role of some synthetic curcuminoid derivatives in the inhibition of tumour specific angiogenesis.

In this study, some of the synthetic curcuminoid derivatives are analyzed for their anti-angiogenic activity. Intraperitoneal administration of the compounds tetrahydrocurcumin (THC), salicyl curcumin (SC) and curcuminIII (C-III) reduced the number of tumour directed capillaries induced by injecting B16F-10 melanoma cells on the ventral side of C57BL/6 mice. THC (14.5 +/- 2.5 capillaries) and SC (16 +/- 2.5 capillaries) were more significant (P < 0.001) than C-III (19 +/- 1.8 capillaries) compared to the untreated control (30.8 +/- 2.1 capillaries). Treatment with these curcuminoids reduced the serum NO as well as TNF-alpha levels of the angiogenesis-induced animals. In vitro NO and TNF-alpha production by the activated MOs were reduced in a concentration dependent manner by the treatment of the curcuminoid compounds.

Angiogenesis Inhibitors↗

PubMed2003

Enhanced release of IL-1beta and TNF-alpha following endotoxin challenge from rat alveolar macrophages cultured in low-mg(2+) medium.

Our previous data have demonstrated that LPS-stimulated alveolar macrophages produce higher levels of IL-1beta and TNF-alpha mRNA in low-Mg(2+) medium than in normal-Mg(2+) medium. In this study, we examined whether the increased mRNA levels are correlated with the release of both cytokines. LPS-stimulated alveolar macrophages released higher amounts of IL-1beta and TNF-alpha in low-Mg(2+) medium than in normal-Mg(2+) medium. The enhanced release of IL-1beta was completely suppressed by pretreatment with verapamil (a calcium entry blocker), U73122 (a phospholipase C inhibitor), W-7 (a calmodulin inhibitor), and curcumin (an activator-protein [AP]-1 inhibitor), and weakly suppressed by dexamethasone (which inhibits nuclear factor [NF]-kappaB and AP-1). On the other hand, the enhanced release of TNF-alpha was completely suppressed by U73122, and strongly suppressed by TMB-8 (which inhibits calcium release from the endoplasmic reticulum) and W-7, and weakly suppressed by pyrrolidine dithiocarbamate (a NF-kappaB inhibitor). From these results, we conclude that the enhanced release of IL-1beta and TNF-alpha from LPS-stimulated alveolar macrophages in low-Mg(2+) medium depends partly on the enhanced synthesis of both cytokines, and occurs partly via identical, and partly via different, signaling pathways.

Animals↗

PubMed1992

[Growth regularities of yujin (Curcuma longa L.)].

Based on the characteristics of leaf, root and tuber growth as well as dry matter accumulation, the ontogeny of Yujin is divided into 4 stages. The growth and correlation among the leaf, root and tuber as well as accumulation of essential oils and curcumins have also been studied.

Curcumin↗

PubMed2003

Regulation of expression of stromyelysin-1 by proinflammatory cytokines in mouse brain astrocytes.

Stromelysin-1 belongs to matrix metalloproteinases responsible for proteolytic degradation of extracellular matrix in many tissues during various diseases, especially those involving inflammation. We studied the induced expression of stromelysin-1 in primary cultures of mouse brain astrocytes stimulated with various cytokines and cellular growth factors. Interleukin-1-beta (IL-1beta), tumor necrosis factor alpha (TNFalpha) and a mixture of IL-1, TNF and epidermal growth factor (EGF) significantly increased the level of stromelysin-1 mRNA in mouse astrocytes while interferon-gamma (IFN-gamma) inhibited this response or was without effect. This accumulation of specific mRNA was preceded by activation of two examined transcription factors: NFkappaB and AP-1. However, experiments with known inhibitors of activation of these transcription factors: pyrrolidine dithiocarbamate (PDTC), parthenolide and curcumin, indicate that NFkappaB and AP-1 cannot be solely responsible for the cytokine induced expression of stromelysin-1 gene in mouse astrocytes.

Animals↗

PubMedDate not supplied

Re-evaluation of cytotoxicity and iron chelation activity of three beta-diketones by semiempirical molecular orbital method.

We investigated the chelating effect of FeCl3 on three beta-diketones, curcumin [1], (-)-3-(trifluoroacetyl)camphor [2] and 3-formylchromone [3], as judged by changes in their cytotoxicity and absorption spectra. Addition of an equimolar concentration of FeCl3 almost completely abrogated the cytotoxicity and changed the pattern of absorption spectra (decrease in the peak height at 430 nm) of [1], without affecting those of [2] and [3]. A semiempirical molecular orbital method (CAChe), based on these experimental data, proposed the estimated structure of [1] chelated with FeCl3 at 1:1 molar ratio. The present study suggests that [1], but not [2] and [3], is an iron chelator.

Cell Line↗

PubMed2005

Nutraceuticals as anti-angiogenic agents: hopes and reality.

Angiogenesis, the formation of new blood vessels from preexisting vascular network is a driving force of organ development in ontogeny, is necessary for ovulation and hair growth, and is prerequisite for proper wound healing. It is also a critical mechanism of numerous diseases, the most important of which are cancer and atherosclerosis. Therefore, modulation of angiogenesis is considered as therapeutic strategies of great importance for human health. Numerous bioactive plant compounds, often referred to as nutraceuticals are recently tested for the potential clinical applications. Among the most frequently studied are resveratrol, a polyphenol present in red-wine and grape-seed, epigallocatechin-3-gallate (EGCG) from green tea and curcumin from Curcuma longa. It is also possible that components of other plants, including the constituents of local food diet may find application for modulation of angiogenesis, provided that their effectiveness will be confirmed in controlled, scientifically validated trials.

Angiogenesis Inhibitors↗

PubMed2005

[Progress on the study of mechanism of the direct action of TCM bioactive components on ovarian cancer].

Both the morbidity and mortality of ovarian cancer, among malignant tumors ot temale genital organs, are quite high. The traditional therapeutic methods on ovarian cancer are surgical operation, chemotherapy, radiotherapy and combination of these methods mentioned above. In recent years, some components of traditional Chinese medicine, such as genistein, semen Coicis, phytosterols, curcumin, quercetin, ginsenoside, etc. have been found to exert anticancer actions of inhibiting proliferation and inducing apoptosis of cancer cells, increasing the sensitivity of patients to chemotherapeutic agents in viva and/or in vitro, the mechanisms involve such aspects as inhibiting activity of key enzymes in cell metabolism, affecting gene expression, antioxidation, and inhibiting tumor angiogenesis, etc. As an adjuvant therapeutic means, the bioactive components of traditional Chinese medicine have broad future of clinical application.

Angiogenesis Inhibitors↗

PubMed2006

Inhibitory effect of cinnamoyl compounds against human malignant cell line.

In the present study, anti-proliferative effects of dietary polyphenolic compounds have been observed and demonstrated the strong anticancer efficacy of curcumin (CMN), an active constituent of dietary spice (turmeric) using human leukemia cancer cell line. CMN inhibited the proliferation of K562 leukemic cells by induction of apoptosis. The current study demonstrated synergy with combination of drug therapy, and suggested that combination of ferulic acid and cisplatin synergistically inhibited cellular proliferation. Cytotoxic synergy was observed independent of the sequence of addition of two drugs to cultured cells. The synergized growth inhibitory effect with cisplatin was probably associated with G2-M arrest in cell cycle progression. These findings suggested that among the cinnamoyl compounds, CMN was most potent and FER appeared to be a better modulating agent on human malignant cell line.

Antineoplastic Agents↗

PubMed2006

[Study on the chemical constituents of Curcuma phaeocaulis].

OBJECTIVE: To investigate the chemical constituents of the rhizome of Curcuma phaeocaulis Val. METHODS: The constituents were isolated by column chromatography and their structures elucidated by chemical properties and spectroscopic analysis. RESULTS: Five compunds have been isolated and identified as isocurcumenol, curcumenol, alpha-spinasterol, curcumin, and beta-sitosterin-3-O-glucoside. CONCLUSION: alpha-Spinasterol and alpha-stediol were isolated from Curcuma phaeocaulis Val. for the first time.

Curcuma↗

PubMed1989

[Determination of boric acid in biological materials by curcuma paper].

The field of legal medicine has seen a recent increase of poisoning by boric acid and, in cases of emergency, a simple method of making a qualitative analysis of the boric acid content is a necessity. Thus, we have examined curcuma paper (turmeric paper) to see if it can provide a qualitative analysis of the boric acid content in biological materials, so as to identify cases of poisoning. It was found that curcuma paper can provide a preliminary analysis of the quantitative content of boric acid, and that about 0.1 mg/ml of boric acid can be determined. The steps for this testing method follow. First, either blood or urine is acidified with a 6 N concentration of hydrochloric acid, i.e., in the case of urine, 0.5 ml of urine is added to 0.1 ml hydrochloric acid, and for blood, 0.5 ml of blood is added to 0.2 ml hydrochloric acid. If the sample is not sufficiently acidic, more hydrochloric acid is added. Next, a drop of the sample is placed on the curcuma paper and, after drying at room temperature, a red stain results if boric acid is present. (Rosocyanin is formed by the reaction of boric acid and protonated curcumin). Then, a 1 N concentration of sodium hydroxide is dropped onto the stained place, and if rosocyanin is present, the stain will turn blue. Informatively, to make curcuma paper, filter paper (No. 2) is soaked in a saturated curcumin/ethanol solution and then air dried.(ABSTRACT TRUNCATED AT 250 WORDS)

Boric Acids↗

PubMed1997

Growth and toxigenesis of Aspergillus flavus isolates on selected spices.

None of the four Aspergillus flavus isolates studied was able to grow on wet cinnamon (5 g cinnamon + 3.3 mL distilled water) at 25 degrees C over 30 days. Fungal growth was weak on the curcumin, black pepper, and white pepper; good, but lower than on rice control, on the cumin and ginger; and similar to the control on sweet and hot paprika. No aflatoxin was detected in black or white pepper after 10 days at 25 degrees C. Cumin least inhibited aflatoxin synthesis, followed by hot paprika, cumin, sweet paprika, and ginger. The amount of aflatoxin detected in the spices at the end of the incubation period never exceeded 6.25% of that found in the rice control.

Aflatoxin B1↗

PubMed1997

A secreted/shed product of Helicobacter pylori activates transcription factor nuclear factor-kappa B.

Helicobacter pylori is an etiologic agent in the development of chronic gastritis, duodenal ulceration, and gastric adenocarcinoma. Exposure of gastric epithelial cells to H. pylori induces secretion of the cytokine IL-8, which plays a pivotal role in the immunopathogenesis of H. pylori infections. Isolated Helicobacter strains differ in their virulence and in their ability to induce cytokine production. High degrees of virulence correlate with enhanced IL-8 production. However, the molecular mechanism of this variance in Helicobacter pathogenicity remains poorly understood. Here we show that H. pylori-mediated IL-8 secretion requires activation of the transcription factor nuclear factor-kappaB (NF-kappaB) in a gastric epithelial cell line. Several H. pylori strains which fail to induce IL-8 secretion do not activate NF-kappaB, while all IL-8-inducing strains activate the transcription factor. Moreover, the antioxidant curcumin, which inhibits NF-kappaB activation, also completely suppresses IL-8 induction by H. pylori. NF-kappaB activation is not mediated by LPSs, since purified H. pylori LPS had no effect on gastric epithelial cells. In contrast, both IL-8 secretion and NF-kappaB activation require a secreted H. pylori product, which is not secreted by strains mutated in picB/cagE, a recently identified putative transport protein.

Antioxidants↗

PubMedDate not supplied

Protective action of plant polyphenols on radiation-induced chromatid breaks in cultured human cells.

The present study was performed to determine whether plant polyphenols can protect human cells against radiation-induced DNA damage manifested as chromatid breaks. Since each chromatid contains a single continuous molecule of double stranded DNA, chromatid breaks represent unrepaired DNA strand breaks. The addition of green or black tea extracts, their polyphenols or curcumin to cultures of human skin fibroblasts or PHA-stimulated blood lymphocytes significantly reduced the frequencies of radiation-induced chromatid breaks. An exception to this general finding was that the green tea polyphenol, (-)epigallocatechin gallate, had no effect. The protective action of these plant polyphenols seems to result from their known antioxidant properties, particularly the scavaging of hydroxyl free radicals. Frequencies of chromatid breaks in cells arrested immediately after irradiation or 0.5 to 1.5 hours post-irradiation in the presence or absence of a DNA repair inhibitor, provide a measure of DNA damage. The results of the present study show that tea and other plant polyphenols can protect human cells against radiation-induced DNA damage.

Catechin↗