Dietary isoflavones suppress endotoxin-induced inflammatory reaction in liver and intestine

Paradkar, Prasad N.; Blum, Penny S.; Berhow, Mark A.; Baumann, Heinz; Kuo, Shiu‐Ming

doi:10.1016/j.canlet.2004.05.019

Cited by 96 publications

(74 citation statements)

References 44 publications

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“…The most important compound in reducing paw edema induced by carrageenan was quercetin [8]. Paradkar et al [19] demonstrated that an isoflavone-containing diet with daidzin, glycitin, genistein and their glucosides, can modulate the inflammatory reaction in the intestine and liver of mice after LPS injection. These in vivo findings were consistent with the anti-inflammatory effect of genistein found in cell studies using human intestinal CACO-2 cells.…”

Section: Flavonoids and Inflammationmentioning

confidence: 99%

“…In particular, tumor necrosis factor-a (TNF-a), IL-6 and IL-1b are prominent contributors to chronic inflammatory responses. Genistein was reported to inhibit IL-1b, IL-6 and TNF-a production in LPS-induced human blood monocytes [54].The inhibitory effect of genistein on IL-6 production has been shown in different settings: cultured human intestinal cells Caco-2 [19], osteoblast cells [91], human gastric epithelial cells [92], or macrophages [93]. Pretreatment of the macrophage cell line RAW 264.7 with luteolin, luteolin-7-glucoside, quercetin, and genistein inhibited both LPS-stimulated TNF-a and IL-6 release, whereas erodictyol and hesperetin only inhibited TNF-a release.…”

Section: Modulation Of the Production Of Other Proinflammatory Moleculesmentioning

confidence: 99%

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Flavonoids as anti-inflammatory agents: implications in cancer and cardiovascular disease

et al. 2009

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Chronic inflammation is being shown to be increasingly involved in the onset and development of several pathological disturbances such as arteriosclerosis, obesity, diabetes, neurodegenerative diseases and even cancer. Treatment for chronic inflammatory disorders has not been solved, and there is an urgent need to find new and safe anti-inflammatory compounds. Flavonoids belong to a group of natural substances occurring normally in the diet that exhibit a variety of beneficial effects on health. The anti-inflammatory properties of flavonoids have been studied recently, in order to establish and characterize their potential utility as therapeutic agents in the treatment of inflammatory diseases. Several mechanisms of action have been proposed to explain in vivo flavonoid anti-inflammatory actions, such as antioxidant activity, inhibition of eicosanoid generating enzymes or the modulation of the production of proinflammatory molecules. Recent studies have also shown that some flavonoids are modulators of proinflammatory gene expression, thus leading to the attenuation of the inflammatory response. However, much work remains to be done in order to achieve definitive conclusions about their potential usefulness. This review summarizes the known mechanisms involved in the anti-inflammatory activity of flavonoids and the implications of these effects on the protection against cancer and cardiovascular disease.

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Section: Flavonoids and Inflammationmentioning

confidence: 99%

Section: Modulation Of the Production Of Other Proinflammatory Moleculesmentioning

confidence: 99%

Flavonoids as anti-inflammatory agents: implications in cancer and cardiovascular disease

et al. 2009

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“…Dietary genistein has been shown to suppress endotoxin-induced inflammatory reaction in liver and intestine [25]. Genistein reportedly protects against a number of human chronic diseases, including cancer and diabetes [26,27].…”

Section: Introductionmentioning

confidence: 99%

Genistein ameliorates cardiac inflammation and oxidative stress in streptozotocin-induced diabetic cardiomyopathy in rats

et al. 2015

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The present study was undertaken to evaluate the protective effects of genistein against cardiac inflammation and oxidative stress in streptozotocin (STZ) (45 mg/kg body weight)-induced diabetic rats. genistein (300 mg/kg/day) was administered orally for 24 weeks to STZ-induced diabetic rats. The effects of genistein on blood glucose, % glycosylated hemoglobin (HbA1c), C-reactive protein, tumor necrosis factor (TNF- α), transforming growth factor (TGF-β1), and total antioxidant were studied. Ultrastructural and histopathological assessment of injury were also undertaken using transmission electron microscope. STZ-induced diabetes resulted in significant increase in the levels of blood glucose, HbA1c, C-reactive protein, TNF- α and TGF-β1, and a decline in total antioxidant reserve of the myocardium. Administration of genistein to diabetic rats resulted in a decrease in blood glucose (p< 0.001), % HbA1c (p < 0.0001), C-reactive protein (p < 0.001), and expression of TNF- α (p < 0.001) and TGF-β1 (p < 0.0001) proteins. In addition, genistein treatment results in augmentation of total antioxidant (p < 0.01) reserve of the hearts. The above findings were supported by histological as well as immunohistochemical localization of NF-κB (p65) in the heart. Genistein treatment ameliorated the ultrastructural degenerative changes in the cardiac tissues as compared to the diabetic control. The result demonstrates that genistein restored the integrity of the diabetic myocardium by virtue of its anti-inflammatory and antioxidant effects.

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“…Genistein protects proinflammatory pathways by inhibiting cytokine-induced overexpression of proinflammatory reactions in human brain microvascular endothelial cells [19]. It also suppresses endotoxin-induced inflammatory reactions in the liver and intestines in vivo [20]. However, the effects of genistein on fractalkine expression and its signaling pathway in endothelial cells, and on CX3CR1 expression in monocytes and macrophages, have not been examined.…”

Section: Introductionmentioning

confidence: 99%

Genistein Suppression of TNF-α-induced Fractalkine Expression in Endothelial Cells

Sung

Kim

Davaatseren

et al. 2010

Cell Physiol Biochem

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Genistein is a polyphenolic nonsteroidal isoflavonoid with estrogen-like activity has been shown to have anticancer, antioxidant, and anti-inflammatory activities. Fractalkine is a unique chemokine that functions as a chemoattractant and an adhesion molecule on endothelial cells activated by proinflammatory cytokines. In this study, we investigated the effects of genistein (5-25 µM) on fractalkine expression in human umbilical vein endothelial cells (HUVECs) and on its receptor, CX3CR1, in THP-1 cells in response to treatment with tumor necrosis factor (TNF)- α. TNF-α significantly induced fractalkine expression in endothelial cells. Genistein decreased TNF-α-induced fractalkine expression through suppression of Akt and p38 phosphorylation and NF-ĸB activities. Genistein also strongly suppressed TNF-α-induced expression of CX3CR1 in monocytes. Genistein suppressed TNF-α-stimulated adhesion of monocytes to HUVECs. Immunohistochemical analysis revealed that genistein suppressed the in vivo lipopolysaccharide (LPS)-induced arterial endothelial fractalkine expression in the heart, kidney, and small intestine. These results suggest that genistein may provide a new pharmacological approach for suppressing fractalkine/CX3CR1-mediated injury under vascular inflammatory conditions.

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Dietary isoflavones suppress endotoxin-induced inflammatory reaction in liver and intestine

Cited by 96 publications

References 44 publications

Flavonoids as anti-inflammatory agents: implications in cancer and cardiovascular disease

Flavonoids as anti-inflammatory agents: implications in cancer and cardiovascular disease

Genistein ameliorates cardiac inflammation and oxidative stress in streptozotocin-induced diabetic cardiomyopathy in rats

Genistein Suppression of TNF-α-induced Fractalkine Expression in Endothelial Cells

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