Curcumin Attenuates Inflammatory Responses of TNF-α-Stimulated Human Endothelial Cells

Kim, Yong Sook; Ahn, Youngkeun; Hong, Moon Hwa; Joo, Soo Yeon; Kim, Kye Hun; Sohn, Il Suk; Park, Hyung Wook; Hong, Young Joon; Kim, Ju Han; Kim, Weon; Jeong, Myung Ho; Cho, Jeong Gwan; Park, Jong Chun; Kang, Jung Chaee

doi:10.1097/fjc.0b013e31805559b9

Cited by 133 publications

(98 citation statements)

References 33 publications

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“…Furthermore, in vitro studies of curcumin have shown the anti-inflammatory Action on human vascular cells. Curcumin attenuates inflammatory response of TNF-α stimulated human endothelial cells by interfering with NF-κB [16,17] and is capable of preventing platelet-derived growth factor (PDGF). It also stimulates the migration of vascular smooth muscle cells (VSMCs) by inhibiting MMP-9 activity and expression [18,19].…”

Section: Cu (Ii) + O 2 −• → Cu (I) + O 2 Cu (I) + H 2 O 2 → Cu (Ii) +mentioning

confidence: 99%

Effect of Curcumin Against Oxidation of Biomolecules by Hydroxyl Radicals

Borra

Mahendra

Gurumurthy

et al. 2014

JCDR

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Background: Among various reactive oxygen species, hydroxyl radicals have the strongest chemical activity, which can damage a wide range of essential biomolecules such as lipids, proteins, and DNA.Objective: The objective of this study was to investigate the beneficial effects of curcumin on prevention of oxidative damage of biomolecules by hydroxyl radicals generated in in vitro by a Fenton like reaction. Materials and Methods:We have incubated the serum, plasma and whole blood with H 2 O 2 /Cu 2 + / Ascorbic acid system for 4 hours at 37 0 C and observed the oxidation of biomolecules like albumin, lipids, proteins and DNA.Results: Curcumin at the concentrations of 50,100 and 200 µmoles, prevented the formation of ischemia modified albumin, MDA, protein carbonyls, oxidized DNA and increased the total antioxidant levels and GSH significantly. Conclusion:These observations suggest the hydroxyl radical scavenging potentials of curcumin and protective actions to prevent the oxidation of biomolecules by hydroxyl radicals.

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Section: Cu (Ii) + O 2 −• → Cu (I) + O 2 Cu (I) + H 2 O 2 → Cu (Ii) +mentioning

confidence: 99%

Effect of Curcumin Against Oxidation of Biomolecules by Hydroxyl Radicals

Borra

Mahendra

Gurumurthy

et al. 2014

JCDR

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“…For example, curcumin inhibits monocyte adhesion by regulation of ROS, expression of adhesion molecules and inhibition of NF-κB activity. This regulation mediates leukocyte adherence in the process of leukocyte trafficking, inhibiting vascular inflammation (12). In the present study, BFNS and EFNS demonstrated inhibition of monocyte adhesion in TNF-α-stimulated endothelial cells and exhibited statistically significant anti-inflammatory activity in a dosedependent manner.…”

Section: Discussionmentioning

confidence: 55%

“…Natural products, which have been traditionally used in the treatment of inflammatory disease, are considered novel and effective biological agents (10)(11)(12)(13). To develop novel therapeutic agents, it is important to investigate the mechanism regulating inflammatory signal reactions.…”

Section: Discussionmentioning

confidence: 99%

“…Won et al reported that cordycepin attenuated neointimal formation by inhibiting reactive oxygen species (ROS)-mediated responses in vascular smooth muscle cells in rats (11). Moreover, some studies have reported that the natural component specifically inhibited the transcriptional activity in the cytokine-stimulated pro-inflammatory response (12,13). Two flavonoids, kaempferol…”

Section: Introductionmentioning

confidence: 99%

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The n-butanol fraction of Naematoloma sublateritium suppresses the inflammatory response through downregulation of NF-κB in human endothelial cells

et al. 2012

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Abstract. Naematoloma sublateritium (Fr.) P. Karst is a chestnut mushroom that is currently a popular edible fungus in the USA, Japan, China and Korea. Although its therapeutic potential in the treatment of diseases has been demonstrated, the pharmacological effect of N. sublateritium (NS) has been poorly studied. In the present study, we demonstrate for the first time that NS suppresses TNF-α-induced inflammatory response in human umbilical vein endothelial cells. The n-butanol fraction of NS (BFNS) inhibited TNF-α-induced monocyte adhesion to endothelial cells in a dose-dependent manner. The anti-adhesive activity of BFNS correlated with suppressed expression of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, monocyte chemoattractant protein-1 and interleukin-8 at both the mRNA and protein levels. In addition, BFNS dose-dependently decreased the expression of inducible nitrogen oxygen synthase (iNOS) and cyclooxygenase-2 (COX-2). Notably, BFNS significantly regulated the nuclear factor (NF)-κB transcriptional activity that was activated by TNF-α stimulation. When considered together, these results suggest that BFNS inhibits the expression of TNF-α-induced adhesion molecules in addition to regulating the iNOS/COX-2 pathways through the modulation of NF-κB in endothelial cells. In conclusion, we propose that BFNS may be a potential therapeutic agent against vascular inflammation, such as atherosclerosis. IntroductionAtherosclerosis, a cardiovascular disease, is a leading cause of death worldwide and is the result of a complicated inflammatory processes on the inner wall of large blood vessels. Immune responses can cause vascular endothelial dysfunctions that eventually disturb blood flow (1). In the early pathogenesis of atherosclerosis, the endothelium is activated by a variety of relevant stimuli, including oxidized lipids, cytokines, or signaling molecules such as endotoxins, and viruses, subsequently expressing specific adhesion receptors that enhance mononuclear cell recruitment into the vessel wall (2,3).The immune reactions in atherosclerotic lesions are mediated by nitric oxide (NO) and cyclooxygenase-2 (COX-2) (4). In the physiological function of the endothelium, NO production is required to inhibit monocyte adhesion and smooth muscle cell chemotaxis and proliferation (5). However, high levels of NO, which are produced by inducible NO synthase (iNOS) in response to stimuli, induce subsequent inflammatory reactions, thus contributing to the progression of atherosclerosis (6). COX-2 has also been associated with pro-atherogenic reactions, generating lipid mediators of inflammation, such as prostaglandin E 2 (PGE 2 ) (7).Epidemiological data continue to support the premise that dietary intake of natural products may improve vascular endothelial dysfunction in both in vivo and in vitro atherosclerotic models (8,9). For example, popular and edible mushrooms have been traditionally used to maintain health, and their components have been used in the prevention and treatment of diseases i...

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“…Although published reports indicate that curcumin effectively inhibits CCL2 expression and secretion in various model systems including human umbilical vein endothelial cells and ex vivo murine pancreatic islets (23,24), the relationship between CCL2 and curcumin has not been studied previously in PCa.…”

Section: Discussionmentioning

confidence: 99%

Curcumin blocks CCL2-induced adhesion, motility and invasion, in part, through down-regulation of CCL2 expression and proteolytic activity

Herman

Stadelman

Roselli³

2009

Int J Oncol

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Abstract. Expression and activity of CC motif ligand 2 (CCL2) is down-regulated by curcumin, the active phytochemical ingredient of turmeric (Curcuma longa), a dietary supplement often self-prescribed to promote prostate health. CCL2 is a potent chemotactic factor of prostate cancer (PCa) with important roles in development of bone metastasis. The relationship between CCL2 and curcumin, however, has not been studied in PCa. Adhesion, invasion and motility of PC-3 cells were measured in response to exposure to curcumin (30 μM; 18 h), CCL2 (100 ng/ml; 18 h) or PMA (100 ng/ml; 18 h). CCL2 mRNA expression and protein secretion levels were measured by real-time PCR and ELISA respectively. Curcumin significantly blocked CCL2 induced adhesion, invasion and motility. Curcumin also significantly suppressed the mRNA expression and secreted CCL2 protein levels. The addition of PMA, a protein kinase C (PKC) activator, blocked the effects of curcumin, leading to an increase in CCL2 expression as well as an increase in PC-3 cell adhesion, invasion and motility. The introduction of a PKC inhibitor, however, blocked the effects of CCL2. We also found that curcumin, CCL2 and PMA, in part, function through the differential regulation of the proteolytic protein matrix metalloproteinase (MMP)-9. These data indicate a potential mechanism; by which curcumin can block the chemotactic effects of CCL2 on PCa. Curcumin exerts potential anti-metastatic effects in bone-derived PCa cells by blocking CCL2 mediated actions on invasion, adhesion and motility, in part through differential regulation of PKC and MMP-9 signaling.

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Curcumin Attenuates Inflammatory Responses of TNF-α-Stimulated Human Endothelial Cells

Cited by 133 publications

References 33 publications

Effect of Curcumin Against Oxidation of Biomolecules by Hydroxyl Radicals

Effect of Curcumin Against Oxidation of Biomolecules by Hydroxyl Radicals

The n-butanol fraction of Naematoloma sublateritium suppresses the inflammatory response through downregulation of NF-κB in human endothelial cells

Curcumin blocks CCL2-induced adhesion, motility and invasion, in part, through down-regulation of CCL2 expression and proteolytic activity

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