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Curcumin Treatment (curcumin + treatment)

Distribution by Scientific Domains

Medical Sciences	37%
Life Sciences	37%

Selected Abstracts

The combination of epigallocatechin gallate and curcumin suppresses ER,-breast cancer cell growth in vitro and in vivo

INTERNATIONAL JOURNAL OF CANCER, Issue 9 2008
Tiffany J. Somers-Edgar
Abstract Both epigallocatechin gallate (EGCG) and curcumin have shown efficacy in various in vivo and in vitro models of cancer. This study was designed to determine the efficacy of these naturally derived polyphenolic compounds in vitro and in vivo, when given in combination. Studies in MDA-MB-231 cells demonstrated that EGCG + curcumin was synergistically cytotoxic and that this correlated with G2/M-phase cell cycle arrest. After 12 hr, EGCG (25 ,M) + curcumin (3 ,M) increased the proportion of cells in G2/M-phase to 263 ± 16% of control and this correlated with a 50 ± 4% decrease in cell number compared to control. To determine if this in vitro result would translate in vivo, athymic nude female mice were implanted with MDA-MB-231 cells and treated with curcumin (200 mg/kg/day, po), EGCG (25 mg/kg/day, ip), EGCG + curcumin, or vehicle control (5 ml/kg/day, po) for 10 weeks. Tumor volume in the EGCG + curcumin treated mice decreased 49% compared to vehicle control mice (p < 0.05), which correlated with a 78 ± 6% decrease in levels of VEGFR-1 protein expression in the tumors. Curcumin treatment significantly decreased tumor protein levels of EGFR and Akt, however the expression of these proteins was not further decreased following combination treatment. Therefore, these results demonstrate that the combination of EGCG and curcumin is efficacious in both in vitro and in vivo models of ER,- breast cancer and that regulation of VEGFR-1 may play a key role in this effect. © 2007 Wiley-Liss, Inc. [source]

Detoxification and antioxidant effects of curcumin in rats experimentally exposed to mercury

JOURNAL OF APPLIED TOXICOLOGY, Issue 5 2010
Rakhi Agarwal
Abstract Curcumin, a safe nutritional component and a highly promising natural antioxidant with a wide spectrum of biological functions, has been examined in several metal toxicity studies, but its role in protection against mercury toxicity has not been investigated. Therefore, the detoxification and antioxidant effects of curcumin were examined to determine its prophylactic/therapeutic role in rats experimentally exposed to mercury (in the from of mercuric chloride-HgCl2, 12,µmol,kg,1 b.w. single intraperitoneal injection). Curcumin treatment (80,mg,kg,1 b.w. daily for 3 days, orally) was found to have a protective effect on mercury-induced oxidative stress parameters, namely, lipid peroxidation and glutathione levels and superoxide dismutase, glutathione peroxidase and catalase activities in the liver, kidney and brain. Curcumin treatment was also effective for reversing mercury-induced serum biochemical changes, which are the markers of liver and kidney injury. Mercury concentration in the tissues was also decreased by the pre/post-treatment with curcumin. However, histopathological alterations in the liver and kidney were not reversed by curcumin treatment. Mercury exposure resulted in the induction of metallothionein (MT) mRNA expressions in the liver and kidney. Metallothionein mRNA expression levels were found to decrease after the pre-treatment with curcumin, whereas post-treatment with curcumin further increased MT mRNA expression levels. Our findings suggest that curcumin pretreatment has a protective effect and that curcumin can be used as a therapeutic agent in mercury intoxication. The study indicates that curcumin, an effective antioxidant, may have a protective effect through its routine dietary intake against mercury exposure. [source]

Curcumin differentially regulates TGF-,1, its receptors and nitric oxide synthase during impaired wound healing

BIOFACTORS, Issue 1-2 2002
Haresh Mani
Abstract Wound healing is a highly ordered process, requiring complex and coordinated interactions involving peptide growth factors of which transforming growth factor-beta (TGF-,) is one of the most important. Nitric oxide is also an important factor in healing and its production is regulated by inducible nitric oxide synthase (iNOS). We have earlier shown that curcumin (diferuloylmethane), a natural product obtained from the plant Curcuma longa, enhances cutaneous wound healing in normal and diabetic rats. In this study, we have investigated the effect of curcumin treatment by topical application in dexamethasone-impaired cutaneous healing in a full thickness punch wound model in rats. We assessed healing in terms of histology, morphometry, and collagenization on the fourth and seventh days post-wounding and analyzed the regulation of TGF-,1, its receptors type I (tIrc) and type II (tIIrc) and iNOS. Curcumin significantly accelerated healing of wounds with or without dexamethasone treatment as revealed by a reduction in the wound width and gap length compared to controls. Curcumin treatment resulted in the enhanced expression of TGF-,1 and TGF-, tIIrc in both normal and impaired healing wounds as revealed by immunohistochemistry. Macrophages in the wound bed showed an enhanced expression of TGF-,1 mRNA in curcumin treated wounds as evidenced by in situ hybridization. However, enhanced expression of TGF-, tIrc by curcumin treatment observed only in dexamethasone-impaired wounds at the 7th day post-wounding. iNOS levels were increased following curcumin treatment in unimpaired wounds, but not so in the dexamethasone-impaired wounds. The study indicates an enhancement in dexamethasone impaired wound repair by topical curcumin and its differential regulatory effect on TGF-,1, it's receptors and iNOS in this cutaneous wound-healing model. [source]

Detoxification and antioxidant effects of curcumin in rats experimentally exposed to mercury

Curcumin-induced fibroblast apoptosis and in vitro wound contraction are regulated by antioxidants and heme oxygenase: implications for scar formation

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 4 2009
A. Scharstuhl
Abstract Fibroblast apoptosis plays a crucial role in normal and pathological scar formation and therefore we studied whether the putative apoptosis-inducing factor curcumin affects fibroblast apoptosis and may function as a novel therapeutic. We show that 25-,M curcumin causes fibroblast apoptosis and that this could be inhibited by co-administration of antioxidants N -acetyl- l -cysteine (NAC), biliverdin or bilirubin, suggesting that reactive oxygen species (ROS) are involved. This is supported by our observation that 25-,M curcumin caused the generation of ROS, which could be completely blocked by addition of NAC or bilirubin. Since biliverdin and bilirubin are downstream products of heme degradation by heme oxygenase (HO), it has been suggested that HO-activity protects against curcumin-induced apoptosis. Interestingly, exposure to curcumin maximally induced HO-1 protein and HO-activity at 10,15 ,M, whereas, at a concentration of >20-,M curcumin HO-1-expression and HO-activity was negligible. NAC-mediated inhibition of 25-,M curcumin-induced apoptosis was demonstrated to act in part via restored HO-1-induction, since the rescuing effect of NAC could be reduced by inhibiting HO-activity. Moreover pre-induction of HO-1 using 5-,M curcumin protected fibroblasts against 25-,M curcumin-induced apoptosis. On a functional level, fibroblast-mediated collagen gel contraction, an in vitro wound contraction model, was completely prevented by 25-,M curcumin, while this could be reversed by co-incubation with NAC, an effect that was also partially HO-mediated. In conclusion, curcumin treatment in high doses (>25 ,M) may provide a novel way to modulate pathological scar formation through the induction of fibroblast apoptosis, while antioxidants, HO-activity and its effector molecules act as a possible fine-tuning regulator. [source]

Curcumin downregulates H19 gene transcription in tumor cells

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 5 2008
Renata Novak Kujund
Abstract Curcumin (diferuloymethane), a natural compound used in traditional medicine, exerts an antiproliferative effect on various tumor cell lines by an incompletely understood mechanism. It has been shown that low doses of curcumin downregulate DNA topoisomerase II alpha (TOP2A) which is upregulated in many malignances. The activity of TOP2A is required for RNA polymerase II transcription on chromatin templates. Recently, it has been reported that CTCF, a multifunctional transcription factor, recruits the largest subunit of RNA polymerase II (LS Pol II) to its target sites genome-wide. This recruitment of LS Pol II is more pronounced in proliferating cells than in fully differentiated cells. As expression of imprinted genes is often altered in tumors, we investigated the potential effect of curcumin treatment on transcription of the imprinted H19 gene, located distally from the CTCF binding site, in human tumor cell lines HCT 116, SW 620, HeLa, Cal 27, Hep-2 and Detroit 562. Transcription of TOP2A and concomitantly H19 was supressed in all tumor cell lines tested. Monoallelic IGF2 expression was maintained in curcumin-treated cancer cells, indicating the involvement of mechanism/s other than disturbance of CTCF insulator function at the IGF2/H19 locus. Curcumin did not alter H19 gene transcription in primary cell cultures derived from normal human tissues. J. Cell. Biochem. 104: 1781,1792, 2008. © 2008 Wiley-Liss, Inc. [source]

Curcumin differentially regulates TGF-,1, its receptors and nitric oxide synthase during impaired wound healing

Modulation of protein kinase C by curcumin; inhibition and activation switched by calcium ions

BRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2007
Y A Mahmmoud
Background and purpose: Previous studies have identified the natural polyphenol curcumin as a protein kinase C (PKC) inhibitor. In contrast, we found significant stimulation of PKC activity following curcumin treatment. Thus, the mechanism of curcumin interaction with PKC was investigated. Experimental approach: We employed phosphorylation assays in the presence of soluble or membrane-bound PKC substrates, followed by SDS,PAGE, autoradiography and phosphorylation intensity measurements. Key results: Curcumin inhibited PKC in the absence of membranes whereas stimulation was observed in the presence of membranes. Further analysis indicated that curcumin decreased PKC activity by competition with Ca2+ stimulation of the kinase, resulting in inhibition of activity at lower Ca2+ concentrations and stimulation at higher Ca2+ concentrations. The role of the membrane is likely to be facilitation of Ca2+ -binding to the kinase, thus relieving the curcumin inhibition observed at limited Ca2+ concentrations. Curcumin was found to mildly stimulate the catalytic subunit of PKC, which does not require Ca2+ for activation. In addition, studies on Ca2+ -independent PKC isoforms as well as another curcumin target (the sarcoplasmic reticulum Ca2+ -ATPase) confirmed a correlation between Ca2+ concentration and the curcumin effects. Conclusions and Implications: Curcumin competes with Ca2+ for the regulatory domain of PKC, resulting in a Ca2+ -dependent dual effect on the kinase. We propose that curcumin interacts with the Ca2+ -binding domains in target proteins. To our knowledge, this is the first study that defines an interaction domain for curcumin, and provides a rationale for the broad specificity of this polyphenol as a chemopreventive drug. British Journal of Pharmacology (2007) 150, 200,208. doi:10.1038/sj.bjp.0706970 [source]