Epigallocatechin gallate protects U937 cells against nitric oxide‐induced cell cycle arrest and apoptosis

Kelly, Melissa R.; Geigerman, Cissy; Loo, George

doi:10.1002/jcb.1097

Cited by 27 publications

(17 citation statements)

References 58 publications

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“…The suppression of NO by EGCG supports the findings of previous study which showed that EGCG inhibited NO-induced apoptosis cell cycle arrest and apoptosis in the U937 human promonocyte cell line [Kelly et al, 2001]. Taken together, these results indicated that EGCG has the capacity to alter signaling pathways intimately involved in apoptosis and MMP gene transcription.…”

Section: Apoptosis and Signal Transduction Pathways: Potential Intervsupporting

confidence: 80%

Pathophysiological Mechanisms in Osteoarthritis Lead to Novel Therapeutic Strategies

Malemud¹,

Islam²,

Haqqi³

2003

Cells Tissues Organs

175

141

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Osteoarthritis (OA) is a debilitating, progressive disease of diarthrodial joints associated with aging. At the molecular level, OA is characterized by an imbalance between anabolic (i.e. extracellular matrix biosynthesis) and catabolic (i.e. extracellular matrix degradation) pathways in which articular cartilage is the principal site of tissue injury responses. The pathophysiology of OA also involves the synovium in that ‘nonclassical’ inflammatory synovial processes contribute to OA progression. Chondrocytes are critical to the OA process in that the progression of OA can be judged by the vitality of chondrocytes and their ability to resist apoptosis. Growth factors exemplified by insulin-like growth factor-1, its binding proteins and transforming growth factor-β contribute to anabolic pathways including compensatory biosynthesis of extracellular matrix proteins. Catabolic pathways are altered by cytokine genes such as interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α) which are upregulated in OA. In addition, IL-1 and TNF-α downregulate extracellular matrix protein biosynthesis while concomitantly upregulating matrix metalloproteinase (MMP) gene expression. When MMPs are activated, cartilage extracellular matrix degradation ensues apparently because levels of endogenous cartilage MMP inhibitors cannot regulate MMP activity. Therapeutic strategies designed to modulate the imbalance between anabolic and catabolic pathways in OA may include neutralizing cytokine activity or MMP gene expression or inhibiting signaling pathways which result in apoptosis dependent on mature caspase activity or mitogen-activated protein kinase (MAPK) activity. MAPK activity appears critical for regulating chondrocyte and synoviocyte apoptosis and MMP genes.

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Section: Apoptosis and Signal Transduction Pathways: Potential Intervsupporting

confidence: 80%

Pathophysiological Mechanisms in Osteoarthritis Lead to Novel Therapeutic Strategies

Malemud¹,

Islam²,

Haqqi³

2003

Cells Tissues Organs

175

141

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“…It has been demonstrated that EGCG can scavenge superoxide and hydroxyl radicals (Guo et al 1996), peroxyl radicals, NO (Kelly et al 2001), carbon-center free radicals, singlet oxygen, lipid free radicals (Zhao et al 2001), and peroxynitrite by preventing nitration of tyrosine. Besides, catechins exert their antioxidant effects through ultra rapid electron transfer from catechins to ROS-induced radical sites on DNA (Anderson et al 2001).…”

Section: Discussionmentioning

confidence: 99%

Protective effects of epigallocatechin gallate following 3-nitropropionic acid-induced brain damage: possible nitric oxide mechanisms

Kumar

2009

Psychopharmacology

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“…Flavonoids have been shown to scavenge NO radicals (17) and to protect U937 cells against NO-induced cell cycle arrest and apoptosis (18).…”

mentioning

confidence: 99%

Neutrophil Restraint by Green Tea: Inhibition of Inflammation, Associated Angiogenesis, and Pulmonary Fibrosis

Donà¹,

Dell’Aica²,

Calabrese

et al. 2003

The Journal of Immunology

304

203

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Neutrophils play an essential role in host defense and inflammation, but the latter may trigger and sustain the pathogenesis of a range of acute and chronic diseases. Green tea has been claimed to exert anti-inflammatory properties through unknown molecular mechanisms. We have previously shown that the most abundant catechin of green tea, (−)epigallocatechin-3-gallate (EGCG), strongly inhibits neutrophil elastase. Here we show that 1) micromolar EGCG represses reactive oxygen species activity and inhibits apoptosis of activated neutrophils, and 2) dramatically inhibits chemokine-induced neutrophil chemotaxis in vitro; 3) both oral EGCG and green tea extract block neutrophil-mediated angiogenesis in vivo in an inflammatory angiogenesis model, and 4) oral administration of green tea extract enhances resolution in a pulmonary inflammation model, significantly reducing consequent fibrosis. These results provide molecular and cellular insights into the claimed beneficial properties of green tea and indicate that EGCG is a potent anti-inflammatory compound with therapeutic potential.

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Epigallocatechin gallate protects U937 cells against nitric oxide‐induced cell cycle arrest and apoptosis

Cited by 27 publications

References 58 publications

Pathophysiological Mechanisms in Osteoarthritis Lead to Novel Therapeutic Strategies

Pathophysiological Mechanisms in Osteoarthritis Lead to Novel Therapeutic Strategies

Protective effects of epigallocatechin gallate following 3-nitropropionic acid-induced brain damage: possible nitric oxide mechanisms

Neutrophil Restraint by Green Tea: Inhibition of Inflammation, Associated Angiogenesis, and Pulmonary Fibrosis

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