Curcumin inhibits cyclooxygenase-2 transcription in bile acid- and phorbol ester-treated human gastrointestinal epithelial cells

Zhang, Fan; Altorki, Nasser K.; Mestre, Juan R.; Subbaramaiah, Kotha; Dannenberg, Andrew J.

doi:10.1093/carcin/20.3.445

Cited by 262 publications

(155 citation statements)

References 38 publications

Supporting

Mentioning

141

Contrasting

Unclassified

Order By: Relevance

“…Accumulating evidences suggest that curcumin inhibits the expression of COX-2 in several experimental models (Zhang et al, 1999;Chun et al, 2003;Surh, 2003;Kang et al, 2004). Consistent with these, through the present study, we have demonstrated that curcumin also effectively inhibits the expressions of COX-2 mRNA and protein induced by UVB irradiation in a human keratinocyte cell line HaCaT, which seems to be, to our knowledge, the first report.…”

Section: Discussionsupporting

confidence: 91%

Curcumin inhibits the expression of COX-2 in UVB-irradiated human keratinocytes (HaCaT) by inhibiting activation of AP-1: p38 MAP kinase and JNK as potential upstream targets

Cho

Park²,

Kweon³

et al. 2005

Exp Mol Med

138

100

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 91%

Curcumin inhibits the expression of COX-2 in UVB-irradiated human keratinocytes (HaCaT) by inhibiting activation of AP-1: p38 MAP kinase and JNK as potential upstream targets

Cho

Park²,

Kweon³

et al. 2005

Exp Mol Med

138

100

View full text Add to dashboard Cite

“…Cells were then treated with fresh 3% fetal bovine serum RPMI with or without LPS (50 ng/ml). Nuclear extracts were obtained 30 min later as described previously (23). Briefly, cells were lysed by incubation in buffer A (10 mM HEPES, pH 7.9, 1.5 mM MgCl 2 , 10 mM KCl, 0.5 mM dithiothreitol, and 0.2 mM phenylmethylsulfonyl fluoride) on ice for 15 min, followed by vortexing for 10 s. Nuclei were pelleted, and nuclear extracts were obtained by high salt extraction after incubating nuclei in buffer C (20 mM HEPES, pH 7.9, 25% glycerol, 420 mM NaCl, 1.5 mM MgCl 2 , 0.2 mM EDTA, 0.5 mM dithiothreitol, and 0.2 mM phenylmethylsulfonyl fluoride) for 20 min.…”

Section: Methodsmentioning

confidence: 99%

Redundancy in the Signaling Pathways and Promoter Elements Regulating Cyclooxygenase-2 Gene Expression in Endotoxin-treated Macrophage/Monocytic Cells

Mestre¹,

Mackrell²,

Rivadeneira³

et al. 2001

Journal of Biological Chemistry

Self Cite

137

View full text Add to dashboard Cite

Macrophage expression of cyclooxygenase-2 (COX-2), the inducible isoform of COX, is up-regulated by proinflammatory stimuli both in vivo and in vitro. Here we investigated the mechanisms regulating COX-2 gene expression in macrophage/monocytic cells. Lipopolysaccharide (LPS) is known to induce de novo COX-2 mRNA expression in these cells. Transient cotransfections with a COX-2 promoter-luciferase construct and different expression vectors showed that LPS up-regulates COX-2 transcription through both mitogen-activated protein kinase (MAPK) and protein kinase C (PKC) pathways. Cotransfections with expression vectors for dominant negative mutants of MAPK and PKC isoforms did not suppress the effects of LPS on COX-2. Electrophoretic mobility shift assays and transient transfection experiments with deleted and mutated variants of a COX-2 promoter-luciferase construct showed that NFB, NF-IL6, and CRE promoter sites mediate gene transcription independently in response to LPS treatment. In these experiments, isolated NFB, NF-IL6, and CRE promoter sites were less effective than the intact promoter in mediating COX-2 transcription. Cotransfections with mutated COX-2 promoter-luciferase constructs and expression vectors showed that each one of these promoter elements can be activated by LPS through both MAPK and PKC pathways to induce gene expression. In summary, there is redundancy in the signaling pathways and promoter elements regulating COX-2 transcription in endotoxin-treated cells of macrophage/ monocytic lineage.

show abstract

“…At least part of the effect of curcumin on inducible PGE 2 production in human blood can be attributed to inhibition of COX2 transcription, which might be due to the inhibition of the NF-B-activating enzymes IKK-␣/␤. 57,58 The effect of curcumin described in an ex vivo assay developed using blood from healthy volunteers 56 was associated with a daily oral dose which furnished plasma levels in the 10 −8 M range in patients with advanced colorectal cancer. 16 This concentration of curcumin is less than a hundredth of that shown in vitro to elicit an effect in blood or colon cells.…”

Section: Dose-effect Relationshipsmentioning

confidence: 99%

Pharmacokinetics and Pharmacodynamics of Curcumin

Sharma¹,

Steward²,

Gescher³

2007

Advances in Experimental Medicine and Biology

385

251

View full text Add to dashboard Cite

Curcuma spp. contain turmerin, essential oils, and curcuminoids, including curcumin. Curcumin [1,7-bis-(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione] is regarded as the most biologically active constituent of the spice turmeric and it comprises 2-8% of most turmeric preparations. Preclinical data from animal models and phase I clinical studies performed with human volunteers and patients with cancer have demonstrated low systemic bioavailability following oral dosing. Efficient first-pass metabolism and some degree of intestinal metabolism, particularly glucuronidation and sulfation of curcumin, might explain its poor systemic availability when administered via the oral route. A daily oral dose of 3.6 g of curcumin is compatible with detectable levels of the parent compound in colorectal tissue from patients with cancer. The levels demonstrated might be sufficient to exert pharmacological activity. There appears to be negligible distribution of the parent drug to hepatic tissue or other tissues beyond the gastrointestinal tract. Curcumin possesses wide-ranging anti-inflammatory and anticancer properties. Many of these biological activities can be attributed to its potent antioxidant capacity at neutral and acidic pH, its inhibition of cell signaling pathways at multiple levels, its diverse effects on cellular enzymes, and its effects on cell adhesion and angiogenesis. In particular, curcumin's ability to alter gene transcription and induce apoptosis in preclinical models advocates its potential utility in cancer chemoprevention and chemotherapy. With regard to considerable public and scientific interest in the use of phytochemicals derived from dietary components to combat or prevent human diseases, curcumin is currently a leading agent.

show abstract

Curcumin inhibits cyclooxygenase-2 transcription in bile acid- and phorbol ester-treated human gastrointestinal epithelial cells

Cited by 262 publications

References 38 publications

Curcumin inhibits the expression of COX-2 in UVB-irradiated human keratinocytes (HaCaT) by inhibiting activation of AP-1: p38 MAP kinase and JNK as potential upstream targets

Curcumin inhibits the expression of COX-2 in UVB-irradiated human keratinocytes (HaCaT) by inhibiting activation of AP-1: p38 MAP kinase and JNK as potential upstream targets

Redundancy in the Signaling Pathways and Promoter Elements Regulating Cyclooxygenase-2 Gene Expression in Endotoxin-treated Macrophage/Monocytic Cells

Pharmacokinetics and Pharmacodynamics of Curcumin

Contact Info

Product

Resources

About