Curcumin (Diferuloylmethane) Inhibition of Tumor Necrosis Factor (TNF)-Mediated Adhesion of Monocytes to Endothelial Cells by Suppression of Cell Surface Expression of Adhesion Molecules and of Nuclear Factor-κB Activation

Kumar, Ashok; Dhawan, Subhash; Hardegen, Neil J.; Aggarwal, Bharat B.

doi:10.1016/s0006-2952(97)00557-1

Cited by 229 publications

(131 citation statements)

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“…How curcumin inhibits the cyclinD1 promoter activity is also not clear. The promoter of cyclin D1 is regulated by NF-kB (Guttridge et al, 1999;Henry et al, 2000;Hinz et al, 1999), and we and others have previously shown that curcumin inhibits NF-kB activation (Singh and Aggarwal, 1995;Kumar et al, 1998;Plummer et al, 1999;Jobin et al, 1999). Thus it is possible that the effect of curcumin on the cyclin D1 mRNA is due to its ability to suppress NF-kB activation.…”

Section: Mcf-7mentioning

confidence: 86%

“…Because NF-kB is known to be down-regulated by curcumin (Singh and Aggarwal, 1995;Kumar et al, 1998;Plummer et al, 1999;Jobin et al, 1999), it is possible that curcumin affects cyclin D1 expression by affecting the cyclin D1 promoter activity. To determine this, cells were transfected with the cyclin D1 promoter-linked to luciferase reporter, treated with 50 mM curcumin, and assayed for the luciferase reporter activity.…”

Section: Curcumin Down-regulates Cyclin D1 Promoter Activitymentioning

confidence: 99%

“…Ras-dependent regulation of cyclin D1 transcription has been shown to occur through a NF-kB activation (Joyce et al, 1999). We and others have previously shown that curcumin (diferuloylmethane), a chemopreventive agent, is a potent down-regulator of NF-kB activation, most likely through the suppression of IkBa kinase (IKK) needed for NF-kB activation and it inhibits NFkB-mediated gene expression (Singh and Aggarwal, 1995;Kumar et al, 1998;Plummer et al, 1999;Jobin et al, 1999). Curcumin is also known to suppress the proliferation of a wide variety of tumor cells, including breast and prostate cancer cells (Mehta et al, 1997;Anto et al, 2002;Kuo et al, 1996;Jiang et al, 1996;Ranjan et al, 1999;Piwocka et al, 1999;Han et al, 1999;Simon et al, 1998;Ramachandran and You, 1999;Bhaumik et al, 1999), through a mechanism which is incompletely understood.…”

Section: Introductionmentioning

confidence: 99%

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Curcumin-induced suppression of cell proliferation correlates with down-regulation of cyclin D1 expression and CDK4-mediated retinoblastoma protein phosphorylation

et al. 2002

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Cyclin D1 is a proto-oncogene that is overexpressed in many cancers including breast and prostate. It plays a role in cell proliferation through activation of cyclin-dependent kinases. Curcumin, a diferuloylmethane, is a chemopreventive agent known to inhibit the proliferation of several breast and prostate cancer cell lines. It is possible that the effect of curcumin is mediated through the regulation of cyclin D1. In the present report we show that inhibition of the proliferation of various prostate, breast and squamous cell carcinoma cell lines by curcumin correlated with the down-regulation of the expression of cyclin D1 protein. In comparison, the down-regulation by curcumin of cyclin D2 and cyclin D3 was found only in selective cell lines. The suppression of cyclin D1 by curcumin led to inhibition of CDK4-mediated phosphorylation of retinoblastoma protein. We found that curcumin-induced down-regulation of cyclin D1 was inhibited by lactacystin, an inhibitor of 26S proteosome, suggesting that curcumin represses cyclin D1 expression by promoting proteolysis. We found that curcumin also down-regulated mRNA expression, thus suggesting transcriptional regulation. Curcumin also inhibited the activity of the cyclin D1 promoter-dependent reporter gene expression. Overall our results suggest that curcumin down-regulates cyclin D1 expression through activation of both transcriptional and post-transcriptional mechanisms, and this may contribute to the antiproliferative effects of curcumin against various cell types.

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Section: Mcf-7mentioning

confidence: 86%

Section: Curcumin Down-regulates Cyclin D1 Promoter Activitymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Curcumin-induced suppression of cell proliferation correlates with down-regulation of cyclin D1 expression and CDK4-mediated retinoblastoma protein phosphorylation

et al. 2002

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“…In VSMCs, LPS has been shown to induce the overexpression of many pro-inflammatory cytokines, including TNF-α, nitric oxide synthase, and MCP-1 [3,31,32] . Cur has been found to inhibit LPS-induced overexpression of vascular cell adhesion molecule-1 (VCAM-1), which plays a critical role in inflammatory responses within atherosclerotic plaques by regulating the [33] . In our study, we found that LPS markedly increased the expression of TNF-α and MCP-1 in VSMCs, which is consistent with findings in previous reports.…”

Section: Wwwchinapharcom Meng Z Et Almentioning

confidence: 99%

Curcumin inhibits LPS-induced inflammation in rat vascular smooth muscle cells in vitro via ROS-relative TLR4-MAPK/NF-κB pathways

et al. 2013

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Aim: To investigate whether curcumin (Cur) suppressed lipopolysaccharide (LPS)-induced inflammation in vascular smooth muscle cells (VSMCs) of rats, and to determine its molecular mechanisms. Methods: Primary rat VSMCs were treated with LPS (1 μg/L) and Cur (5, 10, or 30 μmol/L) for 24 h. The levels of MCP-1, TNF-α, and iNOS were measured using ELISA and real-time RT-PCR. NO level was analyzed with the Griess reaction. Western-blotting was used to detect the activation of TLR4, MAPKs, IκBα, NF-κB p65, and the p47 phox subunit of NADPH oxidase in the cells. Results: Treatment of VSMCs with LPS dramatically increased expression of inflammatory cytokines MCP-1 and TNF-α, expression of TLR4 and iNOS, and NO production. LPS also significantly increased phosphorylation of IκBα, nuclear translocation of NF-κB (p65) and phosphorylation of MAPKs in VSMCs. Furthermore, LPS significantly increased production of intracellular ROS, and decreased expression of p47 phox subunit of NADPH oxidase. Pretreatment with Cur concentration-dependently attenuated all the aberrant changes in LPS-treated VSMCs. The LPS-induced overexpression of MCP-1 and TNF-α, and NO production were attenuated by pretreatment with the ERK inhibitor PD98059, the p38 MAPK inhibitor SB203580, the NF-κB inhibitor PDTC or anti-TLR4 antibody, but not with the JNK inhibitor SP600125. Conclusion: Cur suppresses LPS-induced overexpression of inflammatory mediators in VSMCs in vitro via inhibiting the TLR4-MAPK/ NF-κB pathways, partly due to block of NADPH-mediated intracellular ROS production.

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“…22,23) Although WEC is expected to have similar effects of bisacurone or curcumin, it is uncertain that WEC contains substantial amount of these compounds to show the competence. Therefore, it is meaningful to examine the effect of WEC on adhesion molecules.…”

mentioning

confidence: 99%

A hot water extract ofCurcuma longainhibits adhesion molecule protein expression and monocyte adhesion to TNF-α-stimulated human endothelial cells

Kawasaki¹,

Muroyama²,

Yamamoto³

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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The recruitment of arterial leukocytes to endothelial cells is an important step in the progression of various inflammatory diseases. Therefore, its modulation is thought to be a prospective target for the prevention or treatment of such diseases. Adhesion molecules on endothelial cells are induced by proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), and contribute to the recruitment of leukocytes. In the present study, we investigated the effect of hot water extract of Curcuma longa (WEC) on the protein expression of adhesion molecules, monocyte adhesion induced by TNF-α in human umbilical vascular endothelial cells (HUVECs). Treatment of HUVECs with WEC significantly suppressed both TNF-α-induced protein expression of adhesion molecules and monocyte adhesion. WEC also suppressed phosphorylation and degradation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) induced by TNF-α in HUVECs, suggesting that WEC inhibits the NF-κB signaling pathway.

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Curcumin (Diferuloylmethane) Inhibition of Tumor Necrosis Factor (TNF)-Mediated Adhesion of Monocytes to Endothelial Cells by Suppression of Cell Surface Expression of Adhesion Molecules and of Nuclear Factor-κB Activation

Cited by 229 publications

References 43 publications

Curcumin-induced suppression of cell proliferation correlates with down-regulation of cyclin D1 expression and CDK4-mediated retinoblastoma protein phosphorylation

Curcumin-induced suppression of cell proliferation correlates with down-regulation of cyclin D1 expression and CDK4-mediated retinoblastoma protein phosphorylation

Curcumin inhibits LPS-induced inflammation in rat vascular smooth muscle cells in vitro via ROS-relative TLR4-MAPK/NF-κB pathways

A hot water extract ofCurcuma longainhibits adhesion molecule protein expression and monocyte adhesion to TNF-α-stimulated human endothelial cells

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