Inhibition of NADPH oxidase subunits translocation by tea catechin EGCG in mast cell

Nishikawa, Hirofumi; Wakano, Keiji; Kitani, Seiichi

doi:10.1016/j.bbrc.2007.08.015

Cited by 57 publications

(45 citation statements)

References 18 publications

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“…6A, LTA stimulated a time-dependent increase in translocation of p47 phox from the cytosol to the membrane with a maximal response within 30 min. DPI (a flavoprotein inhibitor) and APO (an inhibitor of translocation of the oxidase subunits) have been shown to prevent p47 phox translocation to the membrane (31,32). This effect is confirmed by our observation that the LTA-stimulated p47 phox translocation was attenuated by pretreatment with DPI or APO (Fig.…”

Section: Involvement Of Nadph Oxidase and Ros Generation In Lta-inducsupporting

confidence: 85%

“…Pretreatment of human alveolar and bronchial epithelial cells with NAc attenuates the injurious effects of hydrogen peroxide (45). In addition, DPI (a flavoprotein inhibitor) and APO (an inhibitor of translocation of the oxidase subunits) have been shown to prevent p47 phox translocation to the membrane (31,32). Therefore, we further investigated the roles of NADPH oxidase and ROS associated with HO-1 expression in response to LTA in HTSMCs, using NAc, DPI, and APO.…”

Section: Discussionmentioning

confidence: 99%

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Lipoteichoic Acid Induces HO-1 Expression via the TLR2/MyD88/c-Src/NADPH Oxidase Pathway and Nrf2 in Human Tracheal Smooth Muscle Cells

Lee¹,

Wang²,

Lee³

et al. 2008

The Journal of Immunology

132

153

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Heme oxygenase‐1 (HO‐1) is a stress‐inducible rate‐limiting enzyme in heme degradation, which confers cytoprotection against oxidative injury and provides a vital function in maintaining tissue homeostasis. Increasing reports have indicated that lipoteichoic acid (LTA) exerts as LPS as an immune system‐stimulating agent and plays a role in the pathogenesis of severe inflammatory responses induced by Gram‐positive bacteria infection. Here, we report that LTA is an inducer of HO‐1 and examine the signaling pathways by which LTA regulates HO‐1 expression in human tracheal smooth muscle cells (HTSMCs). LTA induced HO‐1 protein, mRNA expression, and HO‐1 promoter activity. LTA‐stimulated HO‐1 expression was attenuated by transfection with dominant negative mutants of Toll‐like receptor‐2 (TLR‐2) and MyD88, the NADPH oxidase inhibitor (DPI), the ROS scavenger (NAC), and transfection with siRNAs of Src and NF‐E2‐related factor 2 (Nrf2). LTA‐stimulated c‐Src phosphorylation, translocation of p47phox and Nrf2, and ROS production were attenuated by transfection with dominant negative mutants of TLR‐2, MyD88, and c‐Src, and by pretreatment with DPI or NAC. Further studies revealed that LTA induced TLR‐2, MyD88, c‐Src, and p47phox complex formation. These results demonstrated that in HTSMCs, LTA induced ROS generation through the TLR‐2/MyD88/c‐Src/NADPH oxidase pathway, in turn initiates the activation of Nrf2, and ultimately induces HO‐1 expression.

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Section: Involvement Of Nadph Oxidase and Ros Generation In Lta-inducsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Lipoteichoic Acid Induces HO-1 Expression via the TLR2/MyD88/c-Src/NADPH Oxidase Pathway and Nrf2 in Human Tracheal Smooth Muscle Cells

Lee¹,

Wang²,

Lee³

et al. 2008

The Journal of Immunology

132

153

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“…Green tea polyphenols consist mainly of catechins, including (2)-Epigallocatechin-3-gallate, the most abundant and strongest bioactive compound. EGCG has been shown to lower the incidence of cancers, 3,4 diabetes, 5 arthritis, 6 inflammatory mediator production and 7,8 oxidative stress, 9,10 and to reduce body weight and body fat. 11 EGCG has also been shown to exert anti-inflammatory activity in immune cells.…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-gallate (EGCG) attenuates inflammation in MRL/lpr mouse mesangial cells

et al. 2010

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Epigallocatechin-3-gallate (EGCG), a bioactive component of green tea, has been reported to exert anti-inflammatory effects on immune cells. EGCG is also shown to activate the metabolic regulator, adenosine 5'-monophosphate-activated protein kinase (AMPK). Reports have also indicated that EGCG inhibits the immune-stimulated phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway. The PI3K/Akt/mTOR pathway has been implicated in mesangial cell activation in lupus. Mesangial cells from MRL/lpr lupus-like mice are hyper-responsive to immune stimulation and overproduce nitric oxide (NO) and other inflammatory mediators when stimulated. In our current studies, we sought to determine the mechanism by which EGCG attenuates immune-induced expression of pro-inflammatory mediators. Cultured mesangial cells from MRL/lpr mice were pre-treated with various concentrations of EGCG and stimulated with lipopolysaccharide (LPS)/interferon (IFN)-c. EGCG activated AMPK and blocked LPS/ IFN-c-induced inflammatory mediator production (iNOS expression, supernatant NO and interleukin-6). Interestingly, EGCG attenuated inflammation during AMPK inhibition indicating that the anti-inflammatory effect of EGCG may be partially independent of AMPK activation. Furthermore, we found that EGCG effectively inhibited the immune-stimulated PI3K/Akt/mTOR pathway independently of AMPK, by decreasing phosphorylation of Akt, suggesting an alternate mechanism for EGCG-mediated anti-inflammatory action in mesangial cells. Taken together, these studies show that EGCG attenuated inflammation in MRL/lpr mouse mesangial cells via the PI3K/Akt/mTOR pathway. Our findings suggest a potential therapeutic role for the use of EGCG to regulate inflammation and control autoimmune disease.

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“…EGCG inhibited endothelin-1-stimulated generation of C-reactive protein in vascular smooth muscle cells, which relieved the inflammatory response and oxidative stress by blocking ROS signals and producing an antiatherosclerotic effect [27]. EGCG inhibited cytosolic subunits of NADPH oxidase from translocating into membrane suggesting inhibition of NADPH oxidase activity in cutaneous mastocytoma cells [28]. Flavonoids prevented oxidative stress in activated monocytes.…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin-3-gallate Regulates NADPH Oxidase Expression in Human Umbilical Vein Endothelial Cells

Ahn

Kim

2010

Korean J Physiol Pharmacol

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Vascular NADPH oxidase plays a pivotal role in producing superoxide in endothelial cells and thus acts in the initiation and development of inflammatory cardiovascular diseases such as atherosclerosis. Epigallocatechin-3-gallate (EGCG), the major catechin derived from green tea, has multiple beneficial effects for treating cardiovascular disease but the effect of EGCG on the expression of vascular NADPH oxidase remains unknown. In this study, we investigated the mechanism(s) by which EGCG might inhibit the expression of subunits of NADPH oxidase, namely p47 . Moreover, EGCG did not affect the production of reactive oxygen species induced by Ang II. These data suggest a novel mechanism whereby EGCG might provide direct vascular benefits for treating inflammatory cardiovascular diseases.

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Inhibition of NADPH oxidase subunits translocation by tea catechin EGCG in mast cell

Cited by 57 publications

References 18 publications

Lipoteichoic Acid Induces HO-1 Expression via the TLR2/MyD88/c-Src/NADPH Oxidase Pathway and Nrf2 in Human Tracheal Smooth Muscle Cells

Lipoteichoic Acid Induces HO-1 Expression via the TLR2/MyD88/c-Src/NADPH Oxidase Pathway and Nrf2 in Human Tracheal Smooth Muscle Cells

Epigallocatechin-3-gallate (EGCG) attenuates inflammation in MRL/lpr mouse mesangial cells

Epigallocatechin-3-gallate Regulates NADPH Oxidase Expression in Human Umbilical Vein Endothelial Cells

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