Showing papers on "Curcumin published in 1997"
TL;DR: It was shown that decomposition was pH-dependent and occurred faster at neutral-basic conditions and vanillin, ferulic acid, feruloyl methane were identified as minor degradation products and the amount of vanillin increased with incubation time.
1,452 citations
TL;DR: It is suggested that curcumin is a potent antiproliferative agent for breast tumor cells and may have potential as an anticancer agent.
Abstract: Pharmacologically safe compounds that can inhibit the proliferation of tumor cells have potential as anticancer agents. Curcumin, a diferuloylmethane, is a major active component of the food flavor turmeric (Curcuma longa) that exhibits anticarcinogenic properties in vivo. In vitro, it suppressed c-jun/Ap-1 and NF-kappaB activation and type 1 human immunodeficiency virus long-terminal repeat-directed gene expression. We examined the antiproliferative effects of curcumin against several breast tumor cell lines, including hormone-dependent and -independent and multidrug-resistant (MDR) lines. Cell growth inhibition was monitored by [3H]thymidine incorporation, Trypan blue exclusion, crystal violet dye uptake and flow cytometry. All the cell lines tested, including the MDR-positive ones, were highly sensitive to curcumin. The growth inhibitory effect of curcumin was time- and dose-dependent, and correlated with its inhibition of ornithine decarboxylase activity. Curcumin preferentially arrested cells in the G2/S phase of the cell cycle. Curcumin-induced cell death was neither due to apoptosis nor to any significant change in the expression of apoptosis-related genes, including Bcl-2, p53, cyclin B and transglutaminase. Overall our results suggest that curcumin is a potent antiproliferative agent for breast tumor cells and may have potential as an anticancer agent.
360 citations
TL;DR: Dietary curcumin showed a distinct tendency to counter changes in lipid fractions of liver and liver cholesterol, triglyceride and phospholipid contents were elevated under diabetic conditions and was seen in diabetic animals maintained on high cholesterol diet.
Abstract: Streptozotocin-induced diabetic rats were maintained on 0.5% curcumin containing diet for 8 weeks. Blood cholesterol was lowered significantly by dietary curcumin in these diabetic animals. Cholesterol decrease was exclusively from LDL-VLDL fraction. Significant decrease in blood triglyceride and phospholipids was also brought about by dietary curcumin in diabetic rats. In a parallel study, wherein diabetic animals were maintained on a high cholesterol diet, the extents of hypercholesterolemia and phospholipidemia were still higher compared to those maintained on control diet. Curcumin exhibited lowering of cholesterol and phospholipid in these animals also. Liver cholesterol, triglyceride and phospholipid contents were elevated under diabetic conditions. Dietary curcumin showed a distinct tendency to counter these changes in lipid fractions of liver. This effect of curcumin was also seen in diabetic animals maintained on high cholesterol diet. Dietary curcumin also showed significant countering of renal cholesterol and triglycerides elevated in diabetic rats. In order to understand the mechanism of hypocholesterolemic action of dietary curcumin, activities of hepatic cholesterol-7a-hydroxylase and HMG CoA reductase were measured. Hepatic cholesterol-7a-hydroxylase activity was markedly higher in curcumin fed diabetic animals suggesting a higher rate of cholesterol catabolism.
297 citations
TL;DR: It is concluded that curcumin inhibits colon cancer cell proliferation in vitro mainly by accumulating cells in the G2/M phase and that this effect is independent of its ability to inhibit prostaglandin synthesis.
281 citations
TL;DR: Curcumin is a strong inhibitor of arachidonic acid‐induced edema of mouse ears in vivo and epidermal cyclo oxygengenase and lipoxygenase activities in vitro, and poor circulating bioavailability of curcumin may account for the lack of lung and breast carcinogenesis inhibition.
Abstract: Curcumin (diferuloylmethane), the naturally occurring yellow pigment in turmeric and curry, is isolated from the rhizomes of the plant Curcuma longa Linn. Curcumin inhibits tumorigenesis during both initiation and promotion (post-initiation) periods in several experimental animal models. Topical application of curcumin inhibits benzo[a]pyrene (B[a]P)-mediated formation of DNA-B[a]P adducts in the epidermis. It also reduces 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced increases in skin inflammation, epidermal DNA synthesis, ornithine decarboxylase (ODC) mRNA level, ODC activity, hyperplasia, formation of c-Fos, and c-Jun proteins, hydrogen peroxide, and the oxidized DNA base 5-hydroxymethyl-2'-deoxyuridine (HmdU). Topical application of curcumin inhibits TPA-induced increases in the percent of epidermal cells in synthetic (S) phase of the cell cycle. Curcumin is a strong inhibitor of arachidonic acid-induced edema of mouse ears in vivo and epidermal cyclooxygenase and lipoxygenase activities in vitro. Commercial curcumin isolated from the rhizome of the plant Curcuma longa Linn contains 3 major curcuminoids (approximately 77% curcumin, 17% demethoxycurcumin, and 3% bisdemethoxycurcumin). Commercial curcumin, pure curcumin, and demethoxycurcumin are about equipotent as inhibitors of TPA-induced tumor promotion in mouse skin, whereas bisdemethoxycurcumin is somewhat less active. Topical application of curcumin inhibits tumor initiation by B[a]P and tumor promotion by TPA in mouse skin. Dietary curcumin (commercial grade) inhibits B[a]P-induced forestomach carcinogenesis, N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG)-induced duodenal carcinogenesis, and azoxymethane (AOM)-induced colon carcinogenesis. Dietary curcumin had little or no effect on 4-(methylnitosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung carcinogenesis and 7,12-dimethylbenz[a]anthracene (DMBA)-induced breast carcinogenesis in mice. Poor circulating bioavailability of curcumin may account for the lack of lung and breast carcinogenesis inhibition.
240 citations
TL;DR: Investigation of the chemopreventive action of dietary curcumin on 7,12-dimethylbenz[a]anthracene (DMBA)-initiated and 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted skin tumor formation in male Swiss ablino mice indicates the safety and the anti-carcinogenic effect ofCurcumin in mice.
208 citations
TL;DR: Investigating the effect of curcumin on the TNF alpha induced expression of endothelial Tissue Factor (TF), the central mediator of coagulation known to be controlled by AP-1 and NF-kappa B found that both, NF- kappa B andAP-1 dependent TF expression, were reduced by cur cumin action.
Abstract: The natural occurring pigment curcumin, a major component of the spice tumeric, has been described to have antioxidative, anti-tumorpromoting, anti-thrombotic and anti-inflammatory properties. It appears, that the pleiotropic effects of curcumin are at least partly due to inhibition of the transcription factors NF-kappa B and AP-1. This study investigates the effect of curcumin on the TNF alpha induced expression of endothelial Tissue Factor (TF), the central mediator of coagulation known to be controlled by AP-1 and NF-kappa B. When bovine aortic endothelial cells (BAEC) were preincubated in the presence of curcumin, TNF alpha induced TF gene transcription and expression were reduced. Transient transfection studies with TF-promoter plasmids revealed that both, NF-kappa B and AP-1 dependent TF expression, were reduced by curcumin action. The observed inhibitions were due to distinct mechanisms. Curcumin inhibited TNF alpha induced I kappa B alpha degradation and the nuclear import of NF-kappa B. In contrast, inhibition of AP-1 was due to a direct interaction of curcumin with AP-1-binding to its DNA binding motif. Thus, curcumin inhibits NF-kappa B and AP-1 by two different mechanisms and reduces expression of endothelial genes controlled by both transcription factors in vitro.
172 citations
TL;DR: Curcumin had a strong inhibitory effect on DNA and RNA synthesis in cultured HeLa cells, but there was little or no effect on protein synthesis.
Abstract: The effects of topical applications of very low doses of curcumin (the major yellow pigment in turmeric and the Indian food curry) on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced oxidation of DNA bases in the epidermis and on tumor promotion in mouse skin were investigated. CD-1 mice were treated topically with 200 nmol of 7,12-dimethylbenz[a]anthracene followed one week later by 5 nmol of TPA alone or together with 1, 10, 100 or 3000 nmol of curcumin twice a week for 20 weeks. Curcumin-mediated effects on TPA-induced formation of the oxidized DNA base 5-hydroxymethyl-2'-deoxyuridine (HMdU) and tumor formation were determined. All dose levels of curcumin inhibited the mean values of TPA-induced HMdU formation in epidermal DNA (62-77% inhibition), but only the two highest doses of curcumin strongly inhibited TPA-induced tumor promotion (62-79% inhibition of tumors per mouse and tumor volume per mouse). In a second experiment, topical application of 20 or 100 nmol (but not 10 nmol) of curcumin together with 5 nmol TPA twice a week for 18 weeks markedly inhibited TPA-induced tumor promotion. Curcumin had a strong inhibitory effect on DNA and RNA synthesis (IC50 = 0.5-1 microM) in cultured HeLa cells, but there was little or no effect on protein synthesis.
164 citations
TL;DR: This study indicates that apigenin inhibited PKC by competing with adenosine triphosphate (ATP) and suggested that the suppression of PKC activity and nuclear oncogene expression might contribute to the molecular mechanisms of inhibition of TPA‐induced tumor promotion by Apigenin and curcumin.
Abstract: Apigenin, a less-toxic and non-mutagenic flavonoid, suppressed 12-0-tetradecanoyl-phorbol-13-acetate-(TPA)-mediated tumor promotion of mouse skin. TPA had the ability to activate protein kinase C (PKC) and induced nuclear proto-oncogene expression. Our study indicates that apigenin inhibited PKC by competing with adenosine triphosphate (ATP). Apigenin also reduced the level of TPA-stimulated phosphorylation of cellular proteins and inhibited TPA-induced c-jun and c-fos expression. Curcumin, a dietary pigment phytopolyphenol, is also a potent inhibitor of tumor promotion induced by TPA in mouse skin. When mouse fibroblast cells were treated with TPA alone, PKC translocated from the cytosolic fraction to the particulate fraction. Treatment with 15 or 20 μM curcumin for 15 min inhibited TPA-induced PKC activity in the particulate fraction by 26–60%. Curcumin also inhibited PKC activity in vitro by competing with phosphatidylserine. Curcumin (10 μM) suppressed the expression of c-jun in TPA-treated cells. Fifteen flavonoids were examined for their effects on morphological changes in soft agar and cellular growth in v-H-ras transformed NIH3T3 cells. The results demonstrated that only apigenin, kaempferol, and genistein exhibited the reverting effect on the transformed morphology of these cells. Based on these findings, it is suggested that the suppression of PKC activity and nuclear oncogene expression might contribute to the molecular mechanisms of inhibition of TPA-induced tumor promotion by apigenin and curcumin. J. Cell. Biochem. Suppls. 28/29:39–48. © 1998 Wiley-Liss, Inc.
164 citations
TL;DR: Results indicate the usefulness of antioxidant food additives in ameliorating aflatoxin-induced mutagenicity and carcinogenicity.
149 citations
TL;DR: The data suggest that the combination of curcumin and genistein in the diet have the potential to reduce the proliferation of estrogen-positive cells by mixtures of pesticides or 17-beta estradiol.
TL;DR: The data suggest that the anticarcinogenic and anti-inflammatory properties of curcumin may be related to its ability to inhibit cellular gene expression regulated by transcription factors NF-kappa B, AP-1, and Egr-1.
Abstract: Binding of plasma factor VII(a) to tissue factor (TF) initiates the coagulation cascade. In health, TF is not expressed in endothelial cells. However, endothelial cells express TF in response to lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF alpha), and other biological stimuli. TF expression by endothelial cells is implicated in thrombotic disorders in patients with a variety of clinical disorders. In the present study, we demonstrate that curcumin (diferulolylmethane), a known anticarcinogenic and anti-inflammatory agent, inhibited phorbol 12-myristate 13-acetate (PMA), LPS, TNF alpha, and thrombin-induced TF activity and TF gene transcription in human endothelial cells. The present data show that curcumin prevented the activation of c-Rel/p65, which is essential for TF gene activation in endothelial cells, by impairing the proteolytic degradation inhibitor protein, I kappa B alpha. The data also show that curcumin downregulated AP-1 binding activity. The present studies are the first to demonstrate that PMA, but not LPS, TNF alpha, and thrombin, induced Egr-1 binding to the second serum-responsive region (SRR-2) of TF promoter and that curcumin inhibited the PMA-induced Egr-1 binding to SRR-2. Overall, the data suggest that the anticarcinogenic and anti-inflammatory properties of curcumin may be related to its ability to inhibit cellular gene expression regulated by transcription factors NF-kappa B, AP-1, and Egr-1.
01 Jan 1997
TL;DR: The data suggest that inhibition of MCP-1/JE transcription by curcumin involves blocking of AP-1 and NF-kB activation by IL1 alpha or TNF-alpha.
Abstract: We have previously demonstrated that anti-inflammatory and antioxidant compound curcumin (diferuloyl-methane) inhibits the expression of monocyte chemoattractant protein-1 (MCP-1/JE) in bone marrow stromal cells by suppressing the transcriptional activity of the MCP-1/JE gene. Since both AP-1 (TRE) and NF-kB (kB) binding motifs are present in the promoter of MCP-1/JE gene, we examined the effect of curcumin on IL1 alpha- and TNF-alpha-induced activation of ubiquitous transcription factors AP-1 and NF-kB by electrophoretic mobility shift assay and Western blotting. IL1 alpha and TNF-alpha rapidly induced both AP-1 and NF-kB DNA binding activities in +/+(-)1.LDA11 stromal cells. However, treatment of these cells with curcumin blocked the activation of AP-1 and NF-kB by both cytokines. These data suggest that inhibition of MCP-1/JE transcription by curcumin involves blocking of AP-1 and NF-kB activation by IL1 alpha or TNF-alpha.
TL;DR: In this paper, a series of curcumin derivatives were prepared and the inhibition of carrageenin-induced oedema by these compounds was established, and it was found that the para hydroxy groups in Curcumin are important for antiinflammatory activity.
TL;DR: Although curcumin alone had little or no effect on cellular differentiation, when it was combined with all-trans retinoic acid or 1α,25-dihydroxyvitamin D3 a synergistic effect was observed and it is possible that many dietary chemicals in fruits, vegetables, and other edible plants can prevent cancer by synergizing with endogenously produced stimulators of differentiation.
Abstract: Topical application of curcumin inhibits chemically induced carcinogenesis on mouse skin, and oral administration of curcumin inhibits chemically induced oral, forestomach, duodenal, and colon carcinogenesis. Curcumin and other inhibitors of cyclooxygenase and lipoxygenase are thought to inhibit carcinogenesis by preventing the formation of arachidonic acid metabolites. In contrast to our expectation of a tumorigenic effect of arachidonic acid, we found that treatment of 7,12-dimethylbenz[a]anthracene-initiated mouse skin with very high doses of arachidonic acid twice daily, 5 days a week for 26 weeks, failed to result in tumors. We considered the possibility that some of the cancer chemopreventive effects of curcumin may be related to an effect of this compound on cellular differentiation, and we investigated the effect of curcumin on differentiation in the human promyelocytic HL-60 leukemia cell model system. Although curcumin alone had little or no effect on cellular differentiation, when it was combined with all-trans retinoic acid or 1alpha,25-dihydroxyvitamin D3 a synergistic effect was observed. It is possible that many dietary chemicals in fruits, vegetables, and other edible plants can prevent cancer by synergizing with endogenously produced stimulators of differentiation such as all-trans retinoic acid, 1alpha,25-dihydroxyvitamin D3, and butyrate. More research is needed to test this hypothesis. Administration of green or black tea inhibits carcinogenesis in several animal models, and tumor growth is also inhibited. Several examples were presented of chemopreventive agents that inhibit carcinogenesis in one animal model but enhance carcinogenesis in a different animal model. Greater efforts should be made to understand mechanisms of cancer chemoprevention and to determine whether a potential chemopreventive agent is useful in many experimental settings or whether it is useful in only a limited number of experimental settings.
TL;DR: The capacity of curcumin to inhibit both cell growth and death strongly implies that these two biological processes share a common pathway at some point and thatCurcumin affects a common step, presumably involving a modulation of the AP-1 transcription factor.
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TL;DR: Investigation of the effect of curcumin on the expression of monocyte chemoattractant protein-1 (MCP-1 or M CP-1/JE) and interferon inducible protein-10kD (IP-10) in mouse bone marrow stromal cell line +/+-1 indicates that whileCurcumin may post-transcriptionally stabilize mRNA transcripts formed in its presence, the overall reduction in mRNA levels by cur cumin is mediated
TL;DR: The ability of curcumin, a natural antioxidant from turmeric, to inhibit radiation-induced lipid peroxidation in rat liver microsomes was examined and it was observed that the antioxidant has significant time- and concentration-dependent inhibitory effect on lipid per oxidation induced by r-radiation.
TL;DR: The data suggest that curcumin treatment reduces the development of BLM-induced inflammatory and oxidant activity, and offers the potential for a novel pharmacological approach in the suppression of drug or chemical-induced lung injury.
TL;DR: It is demonstrated that curcumin and capsaicin can control the release of inflammatory mediators such as eicosanoids and hydrolytic enzymes secreted by macrophages and thereby may exhibit antiinflammatory properties.
Abstract: The inflammatory mediators secreted by macrophages play an important role in autoimmune diseases. Spice components, such as curcumin from turmeric and capsaicin from red pepper, are shown to exhibit antiinflammatory properties. The influence of these spice components on arachidonic acid metabolism and secretion of lysosomal enzymes by macrophages was investigated. Rat peritoneal macrophages preincubated with 10 microM curcumin or capsaicin for 1 h inhibited the incorporation of arachidonic acid into membrane lipids by 82 and 76%: prostaglandin E2 by 45 and 48%; leukotriene B4 by 61 and 46%, and leukotriene C4 by 34 and 48%, respectively, but did not affect the release of arachidonic acid from macrophages stimulated by phorbol myristate acetate. However, the secretion of 6-keto PG F1 alpha was enhanced by 40 and 29% from macrophages preincubated with 10 microM curcumin or capsaicin, respectively, as compared to those produced by control cells. Curcumin and capsaicin also inhibited the secretion of collagenase, elastase, and hyaluronidase to the maximum extent of 57, 61, 66%, and 46, 69, 67%, respectively. These results demonstrated that curcumin and capsaicin can control the release of inflammatory mediators such as eicosanoids and hydrolytic enzymes secreted by macrophages and thereby may exhibit antiinflammatory properties.
TL;DR: Results indicate that curcumin may have a potential effect on controlling allergic diseases through inhibiting the production of cytokines affecting eosinophil function and IgE synthesis.
TL;DR: It is suggested that TPA treatment induces cellular transformation by other unknown routes, because some tested compounds have an inhibitory effect on TPA-induced transformation but have no or a slight inhibitory effects on PKC activation, active oxygen species production, and c-jun induction.
Abstract: The effects of 12 phytopolyphenols, including 3 catechin derivatives, 8 flavanols, and curcumin, on 12–0‐tetradecanoylphorbol 13‐acetate (TPA)‐induced transformation in mouse fibroblast cells are described. The location of hydroxyl functional groups at 2’, 3’, or 4’ site(s), especially at the 4’ site, as in apigenin, fisetin, morin, myricetin, and quercetin, seems essential for anti‐TPA‐induced transformation, anti‐protein kinase C (PKC) activation, and anti‐TPA‐induced c‐jun expression activities. Among the catechin derivatives, those with a cis form structure and with an additional hydroxyl group at the R1 site and galloyl groups at the R2 site, such as epigallocatechin gallate, have stronger inhibitory effects on the above‐mentioned biochemical activities. Considering their polarities and chemical structures, these compounds have different oxygen radical absorbance capacity in the in vitro assay. In addition, curcumin also has these inhibitory effects on the above‐mentioned biochemical activit...
Journal Article•
TL;DR: The results indicate that curcumin is a weak stimulator of differentiation in HL-60 cells and that is has synergistic effects when combined with RA or vitamin D3.
Abstract: Treatment of human promyelocytic leukemia HL-60 cells with 10 muM curcumin for 48 h inhibited cellular proliferation and induced small increases in differentiation (100-200%) as measured by the proportion of cells that reduced nitroblue tetrazolium (NBT) and expressed Mac-1. Synergistic induction of differentiation as measured by the above markers was observed when 1-10 muM curcumin was combined with 10-100 nM all-trans retinoic acid (RA) or with 100 nM 1 alpha, 25-dihydroxyvitamin D3 (vitamin D3). Cell morphology and flow cytometric studies (with the monocytic surface antigen CD14) indicated that combinations of RA and curcumin stimulated differentiation predominantly to granulocytes whereas combinations of vitamin D3 and curcumin stimulated differentiation predominantly to monocytes. Studies on cell cycle kinetics indicated that treatment of HL-60 cells with a combination of RA and curcumin for 48 or 96 h reduced the proportion of cells in the S phase of the cell cycle and increased the proportion of cells in the G0/G1 phase of the cell cycle to a greater extent than occurred for cells treated with either compound alone. Combinations of vitamin D3 and curcumin did not alter cell cycle kinetics to a greater extent than was observed for either compound alone. Combinations of RA and curcumin or vitamin D3 and curcumin inhibited the proliferation of HL-60 cells to a greater extent than was observed for either compound alone. The results indicate that curcumin is a weak stimulator of differentiation in HL-60 cells and that is has synergistic effects when combined with RA or vitamin D3. Combinations of curcumin and RA have a particularly potent inhibitory effect on the proliferation of HL-60 cells.
TL;DR: The results suggest that the anti‐inflammatory and anti‐carcinogenic action of curcumin is partly due to the inhibition of PLD.
TL;DR: In vitro incubation of YAC-1 and EL4 tumor cells and normal splenocytes in varying concentrations of curcumin for varying times revealed differences between cell types inCurcumin's effects on cell proliferation and viability.
Abstract: The effects of dietary curcumin on three major types of immune function were examined in rats. Antibody (IgG) production, delayed-type hypersensitivity and natural killer cell activity were evaluated after 5 weeks of dietary exposure to 1, 20 or 40 mg/kg curcumin. The highest dose of curcumin significantly enhanced IgG levels. Rats receiving lower dietary concentrations (1 or 20 mg/kg) of curcumin were not different in IgG production from rats receiving no curcumin in their diet. Neither delayed-type hypersensitivity nor natural killer cell activity was different from control values at any dietary concentration of curcumin. In vitro incubation of YAC-1 and EL4 tumor cells and normal splenocytes in varying concentrations of curcumin for varying times revealed differences between cell types in curcumin's effects on cell proliferation and viability. No cytotoxic effect was seen in EL4 cells at 12S μg/ml curcumin at 4, 24 and 48 hrs incubations, however, cell proliferation was reduced by almost 50 % a...
TL;DR: Results suggest that some phenolic antioxidants may prevent tissue destruction by preventing the formation of 3-nitrotyrosine in peroxynitrite-modified collagen.
Abstract: To investigate the prevention of protein modification by food components, effects of natural antioxidants on in vitro modification of collagen by peroxynitrite were examined using a polyclonal antibody specific to 3-nitrotyrosine. To perform the assay with many samples at a time, the inhibitory effects of antioxidants were evaluated using an enzyme-linked immunosorbent assay. Polyphenols such as caffeic acid, curcumin, and flavonoids showed strong inhibitory effects on the formation of 3-nitrotyrosine in peroxynitrite-modified collagen. The inhibitory effects of caffeic acid and its related compounds on nitration of Tyr were then further investigated. Both caffeic acid, ferulic acid, and p-coumaric acid inhibited the modification, whereas cinnamic acid did not. By the treatment of p-coumaric acid with peroxynitrite, nitrated p-coumaric acid was detected in the reaction mixture using a liquid chromatograph-mass spectrometer (LC-MS). These results suggest that some phenolic antioxidants may prevent tissue i...
Journal Article•
TL;DR: Curcumin caused a marked reduction in NF-kappa B activity in nuclear extracts of HL-60 cells exposed to this agent in the presence or absence of vitamin D3, supporting the possibility that NF- kappa B may be a factor in the regulation of the state of differentiation of leukemia cells.
Abstract: Previous studies have shown that an antisense phosphorothioate oligonucleotide to the Rel A subunit of NF- kappa B, as well as vitamin E and related antioxidants, significantly enhanced the differentiation of HL-60 leukemia cells when combined with low levels of 1 alpha, 25-dihydroxyvitamin D3 (vitamin D3) an effect accompanied by a marked inhibition of the transcription factor, NF-kappa B. Curcumin, a potent inhibitor of tumor promotion and of tumor cell growth, has also been shown to have antioxidant properties and to inhibit NF-kappa b. to ascertain whether curcumin would also enhance the differentiation of HL-60 leukemia cells produced by vitamin D3, presumably by interfering with NF- kappa B activity, the effects of curcumin on the differentiation of HL-60 cells produced by low levels of vitamin D3 were measured. Curcumin used alone did not produce a significant degree of differentiation of HL-60 cells; however, this agent markedly enhanced the expression of differentiation markers induced by low levels of vitamin D3. Curcumin also increased the differentiation of HL-60 cells when combined with vitamin D analogues (1,25-dihydroxy-16-ene-23-yne vitamin D3 and 1,25-dihydroxy-16-ene vitamin D3) that share the receptor binding properties of vitamin D3, whereas as vitamin D analogue (1,25-dihydroxy-16,23-diene vitamin D3) that caused significant calcium mobilization, but was less effective than vitamin d3 in binding the receptor, did not cause the differentiation of HL-60 cells in the presence or absence of curcumin. Several dietary compounds structurally related to curcumin (i.e., caffeic acid, chlorogenic acid, and ferulic acid) did not increase the differentiation of HL-60 cells produced by vitamin D3. However, the more lipophilic ethyl of ferulic and caffeic acid were capable of inducing the differentiation of HL-60 cells, as well as enhancing the maturation produced by vitamin D3. Curcumin caused a marked reduction in NF-kappa B activity in nuclear extracts of HL-60 cells exposed to this agent in the presence or absence of vitamin D3, supporting the possibility that NF-kappa B may be a factor in the regulation of the state of differentiation of leukemia cells.
TL;DR: In this article, the effects of new complex curcuminoids (cassumunin A and cassumunin B) isolated from tropical ginger, Zingiber cassumunar, were examined in dissociated rat thymocytes suffering from oxidative stress induced by 3 mM hydrogen peroxide by using a flow cytometer and ethidium bromide.
TL;DR: This preliminary experiment suggests that the Curcuma phenolic antioxidants, because of their high antioxidant activity and lack of toxicity, might be a useful complement to standard hypo-lipidemic drugs in the prevention and treatment of atherosclerosis.
Abstract: Extracts from the rhyzome of Curcuma longa are widely used as food additives in India and other Asiatic and Central American countries. It has been shown that these extracts (“turmeric”), as well as “curcumin” and related phenolic compounds isolated from Curcuma, have a powerful antioxidant action when tested in in vitro systems. Moreover, previous research from our laboratories has shown significant decreases in the levels of lipid peroxides in the blood of both mice and human subjects administered “turmeric.” Our present research complements the previous data, showing that a daily intake of turmeric equivalent to 20 mg of the phenolic antioxidant curcumin for 60 days decreases the high levels of peroxidation of both the HDL and the LDL, in vivo, in 30 healthy volunteers ranging in age from 40 to 90 years. The effect was quite striking in the persons with high baseline values of peroxidized compounds in these lipoproteins, while no apparent change took place in the persons having low baseline values.
In view of current concepts on the atherogenic role played by peroxidized HDL, and especially by peroxidized LDL, as inducers of foam and smooth cell proliferation in the arterial wall, this preliminary experiment suggests that the Curcuma phenolic antioxidants, because of their high antioxidant activity and lack of toxicity, might be a useful complement to standard hypo-lipidemic drugs in the prevention and treatment of atherosclerosis.
TL;DR: Curcumin and turmeric fed group showed a significant increase in the abnormally reduced fatty acid levels.
Abstract: The effect of retinol deficiency and curcumin/turmeric on lipid peroxidation and fatty acid profile was studied in liver, kidney, spleen and brain microsomes of rats. Results revealed an increase in lipid peroxidation in retinol deficient liver by 32%, kidney 30%, spleen 24% and brain 43% compared to the controls. Feeding 0.1% curcumin or turmeric for three weeks in diet to retinol deficient rats reduced the lipid peroxidation respectively to 12.5 or 22.6%, in liver, 23.7 or 24.1% in kidney, 14.4 or 18.0% in spleen and 16.0 or 31.4% in brain. Retinol deficiency lead to a reduction in the essential fatty acids. In liver C18:1 showed a reduction by 45.6%, C18:2 by 31.6% and C20:4 by 22.8%. In kidney C18:1 was reduced by 33.6%, 18:2 by 24.6% and 20:4 by 13.7%. In spleen and brain C18:1 showed a reduction by 10.2% and 33.9%, C18:2 by 37.9% and 12.1% and C20:4 by 15.7% and 35.3% respectively. Curcumin and turmeric fed group showed a significant increase in the abnormally reduced fatty acid levels.