(‐)‐Epigallocatechin Gallate Inhibits Endothelin‐1‐Induced C‐Reactive Protein Production in Vascular Smooth Muscle Cells

Wang, Chenjing; Liu, Juntian; Guo, Fang

doi:10.1111/j.1742-7843.2010.00557.x

Cited by 11 publications

(5 citation statements)

References 27 publications

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“…This is consistent with a positive association (not significant) seen between CO and VEGF, in this work (Additional file 1 : Table S1). Meanwhile, in this work UFP is associated with increased plasma endothelin (ET-1) (Table 7 ) and increasing trend (not significant) in CRP (Additional file 1 : Table S1), and ET-1 is known to induce CRP via MAPK signaling in vascular smooth muscle cells and effect vasopressor responses [ 77 ]. These results are consistent with the positive associations seen between UFP and heart rate, as well as CRP and heart rate.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular and inflammatory mechanisms in healthy humans exposed to air pollution in the vicinity of a steel mill

et al. 2018

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BackgroundThere is a paucity of mechanistic information that is central to the understanding of the adverse health effects of source emission exposures. To identify source emission-related effects, blood and saliva samples from healthy volunteers who spent five days near a steel plant (Bayview site, with and without a mask that filtered many criteria pollutants) and at a well-removed College site were tested for oxidative stress, inflammation and endothelial dysfunction markers.MethodsBiomarker analyses were done using multiplexed protein-array, HPLC-Fluorescence, EIA and ELISA methods. Mixed effects models were used to test for associations between exposure, biological markers and physiological outcomes. Heat map with hierarchical clustering and Ingenuity Pathway Analysis (IPA) were used for mechanistic analyses.ResultsMean CO, SO2 and ultrafine particles (UFP) levels on the day of biological sampling were higher at the Bayview site compared to College site. Bayview site exposures “without” mask were associated with increased (p < 0.05) pro-inflammatory cytokines (e.g IL-4, IL-6) and endothelins (ETs) compared to College site. Plasma IL-1β, IL-2 were increased (p < 0.05) after Bayview site “without” compared to “with” mask exposures. Interquartile range (IQR) increases in CO, UFP and SO2 were associated with increased (p < 0.05) plasma pro-inflammatory cytokines (e.g. IL-6, IL-8) and ET-1(1–21) levels. Plasma/saliva BET-1 levels were positively associated (p < 0.05) with increased systolic BP. C-reactive protein (CRP) was positively associated (p < 0.05) with increased heart rate. Protein network analyses exhibited activation of distinct inflammatory mechanisms after “with” and “without” mask exposures at the Bayview site relative to College site exposures.ConclusionsThese findings suggest that air pollutants in the proximity of steel mill site can influence inflammatory and vascular mechanisms. Use of mask and multiple biomarker data can be valuable in gaining insight into source emission-related health impacts.Electronic supplementary materialThe online version of this article (10.1186/s12989-018-0270-4) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Cardiovascular and inflammatory mechanisms in healthy humans exposed to air pollution in the vicinity of a steel mill

et al. 2018

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“…EGCG has been shown to attenuate oxidative stress in human VSMCs via activation of heme oxygenase-1 39 . In addition, EGCG can relieve oxidative stress by inhibiting endothelin-1-stimulated generation of C-reactive protein in VSMCs 40 . In the present study, we demonstrated that EGCG strongly protected against H 2 O 2 -induced VSMCs apoptosis via activation of caspase family and Bcl-2 signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor

Xue

et al. 2017

Sci Rep

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Epigallocatechin-3-gallate (EGCG) is one of the major polyphenolic compounds present in green tea extracts and has been used as a potential drug for the treatment of numerous diseases. The present study aimed to elucidate the role and mechanism of EGCG in protecting against H2O2-induced apoptosis in mouse vascular smooth muscle cells (VSMCs). VSMCs were pretreated with various concentrations of EGCG for 2 hours prior to treatment with H2O2. Treatment with H2O2 significantly decreased the cell viability and induced apoptosis of VSMCs, which were attenuated by pretreatment with EGCG. In particular, EGCG pretreatment significantly inhibited the H2O2-induced upregulation of cleaved forms of caspase-3, caspase-8, and caspase-9, Bax, CathepsinD, and downregulation of Bcl-2. Moreover, the antioxidation effect of EGCG on VSMCs was determined to be associated with the 67kD laminin receptor (67LR). Our results demonstrated that EGCG improved cell viability and protected VSMCs against oxidative stress through both extrinsic and intrinsic pathways, while 67LR is likely to be an active and key receptor of EGCG. These findings provide a novel molecular mechanism of EGCG in inhibiting H2O2-induced apoptosis in VSMCs, as well as its function in preventing the development of atherosclerosis.

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“…EGCG decreased the risk of cardiovascular disease by reducing inflammatory markers in rats fed an atherogenic diet [26]. 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].…”

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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(‐)‐Epigallocatechin Gallate Inhibits Endothelin‐1‐Induced C‐Reactive Protein Production in Vascular Smooth Muscle Cells

Cited by 11 publications

References 27 publications

Cardiovascular and inflammatory mechanisms in healthy humans exposed to air pollution in the vicinity of a steel mill

Cardiovascular and inflammatory mechanisms in healthy humans exposed to air pollution in the vicinity of a steel mill

Epigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor

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

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