Allicin inhibits spontaneous and TNF-? induced secretion of proinflammatory cytokines and chemokines from intestinal epithelial cells

Lang, Alon; Lahav, Maor; Sakhnini, Emad; Barshack, Iris; Fidder, Herma H.; Avidan, Benjamin; Bardan, Eytan; Hershkoviz, Rami; Bar‐Meir, Simon; Chowers, Yehuda

doi:10.1016/j.clnu.2004.03.011

Cited by 164 publications

(67 citation statements)

References 47 publications

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“…The NFjB heterodimer is retained in the cytoplasm in an inactive form through association with one of the IjBs inhibitory proteins. As a consequence of stimulation by TNF-a, the IjBa gets phosphorylated by a specific kinase complex (IKK) leading to its ubiquitination, and subsequent proteolysis by the 28S proteosome [32,33]. The degradation of IjB releases active NF-jB, which translocates to the nucleus and regulates gene expression by binding to jB binding sites or by interacting with other transcriptional factors [34].…”

Section: Discussionmentioning

confidence: 99%

Suppression of Mycobacterium tuberculosis induced reactive oxygen species (ROS) and TNF‐α mRNA expression in human monocytes by allicin

et al. 2006

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Chronic inflammation associated with tumor necrosis factor (TNF)-a and reactive oxygen species (ROS) is the hallmark of tuberculosis. Mycobacterium tuberculosis (MTB) directly stimulates human monocytes to secrete TNF-a. We show the augmented expression of TNF-a mRNA in MTB-infected monocytes by cellular activation and ROS was suppressed by allicin in a dose-dependent manner. Also, allicin enhanced the glutathione peroxidase activity, which correlated inversely with the downregulation of ROS and TNF-a in MTB-infected monocytes. Hence, allicin may prove to be a valuable natural antioxidant in combating tuberculosis.

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Section: Discussionmentioning

confidence: 99%

Suppression of Mycobacterium tuberculosis induced reactive oxygen species (ROS) and TNF‐α mRNA expression in human monocytes by allicin

et al. 2006

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“…Figure 6C shows that IL-8 production increased dose-dependently. Intestinal epithelial cell lines such as Caco-2 and HT-29 are known to spontaneously secrete IL-8 [38,40]. Nontreated control Caco-2 cells released 16.270.3 pg/mL of IL-8.…”

Section: Effect Of Hemin On Il-8 Mrna Expression and Il-8 Production mentioning

confidence: 99%

“…IL-8 production in intestinal epithelial cells increases in response to pro-inflammatory cytokines such as tumor necrosis factor-a [37,38] and IL-1 [32], or oxidative stress such as that by H 2 O 2 [32,39,40]. To determine whether We next treated Caco-2 cells with hemin at various concentrations for 24 h, and the culture medium was collected for IL-8 determination by ELISA.…”

Section: Effect Of Hemin On Il-8 Mrna Expression and Il-8 Production mentioning

confidence: 99%

Heme induces DNA damage and hyperproliferation of colonic epithelial cells via hydrogen peroxide produced by heme oxygenase: A possible mechanism of heme‐induced colon cancer

Ishikawa

Tamaki

Ohata

et al. 2010

Molecular Nutrition Food Res

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Epidemiological and animal model studies have suggested that high intake of heme, present in red meat, is associated with an increased risk of colon cancer. However, the mechanisms underlying this association are not clear. This study aimed to investigate whether heme induces DNA damage and cell proliferation of colonic epithelial cells via hydrogen peroxide produced by heme oxygenase (HO). We examined the effects of zinc protoporphyrin (ZnPP; a HO inhibitor) and catalase on DNA damage, cell proliferation, and IL-8 production induced by the addition of hemin (1-10 microM) to human colonic epithelial Caco-2 cells. DNA damage was determined with a comet assay, and cell proliferation was evaluated with 5-bromo-2'-deoxyuridine incorporation assay. Both ZnPP and exogenous catalase inhibited the hemin-induced DNA damage and cell hyperproliferation dose-dependently. IL-8 messenger RNA expression and IL-8 production in the epithelial cells increased following the hemin treatment, but the production was inhibited by ZnPP and catalase. These results indicate that hemin has genotoxic and hyperproliferative effects on Caco-2 cells by HO and hydrogen peroxide. The mechanism might explain why a high intake of heme is associated with increased risk of colon cancer.

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“…We therefore examined the effect of polyozellin on TNF-α-induced IL-8 levels. The level of IL-8 secretion by HT-29 cells was significantly increased by the addition of TNF-α (Lang et al, 2004). We therefore examined whether polyozellin could suppress the TNF-α-induced IL-8 expression.…”

Section: Effect Of Polyozellin On Tnf-α-induced Il-8 Expression In Htmentioning

confidence: 99%

Polyozellin blocks tumor necrosis factor α-induced interleukin 8 and matrix metalloproteinase 7 production in the human intestinal epithelial cell line HT-29

et al. 2011

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Polyozellin isolated from Polyozellus multiplex (Thelephoraceae) displays potent anti-inflammatory effects in murine macrophages. Here we evaluated whether polyozellin has the potential to ameliorate diseases characterized by mucosal inflammation in intestinal epithelial HT-29 cells. Polyozellin significantly inhibited tumor necrosis factor (TNF)-α-induced interleukin-8 secretion and mRNA expression. Moreover, polyozellin suppressed the expression of matrix metalloproteinase-7 mRNA and extracellular pro-matrix metalloproteinase-7 secretion. A signal transduction study revealed that polyozellin significantly attenuates TNF-α-mediated p38 phosphorylation, inhibitory factor κBα degradation, and nuclear factor-κB-mediated transcriptional activation. Collectively, these results suggest that polyozellin has the potential to attenuate intestinal inflammation and shed light on the novel signal pathway evoked by TNF-α during intestinal inflammation.

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Allicin inhibits spontaneous and TNF-? induced secretion of proinflammatory cytokines and chemokines from intestinal epithelial cells

Cited by 164 publications

References 47 publications

Suppression of Mycobacterium tuberculosis induced reactive oxygen species (ROS) and TNF‐α mRNA expression in human monocytes by allicin

Suppression of Mycobacterium tuberculosis induced reactive oxygen species (ROS) and TNF‐α mRNA expression in human monocytes by allicin

Heme induces DNA damage and hyperproliferation of colonic epithelial cells via hydrogen peroxide produced by heme oxygenase: A possible mechanism of heme‐induced colon cancer

Polyozellin blocks tumor necrosis factor α-induced interleukin 8 and matrix metalloproteinase 7 production in the human intestinal epithelial cell line HT-29

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