Genipin Selectively Inhibits TNF-α-activated VCAM-1 But Not ICAM-1 Expression by Upregulation of PPAR-γ in Human Endothelial Cells

Hwa, Jung Seok; Mun, Lidiya; Kim, Hye Jung; Seo, Han Geuk; Lee, Jae Heun; Kwak, Jong Hwan; Lee, Dong‐Ung; Chang, Ki Churl

doi:10.4196/kjpp.2011.15.3.157

Cited by 25 publications

(21 citation statements)

References 20 publications

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“…This result was consistent with the previous studies [Hwa et al, 2011;Kim et al, 2005]. The fl uorescent intensity was not signifi cantly different from that of control 2 when 30 μg/L of EOF was used, which suggested that the removal effect of ROS was not distinct.…”

Section: Removal Of Rossupporting

confidence: 82%

Polyphenol Profiles and Antioxidant Properties of Ethanol Extracts from Osmanthus Fragrans (Thunb.) Lour. Flowers

Li¹,

Chai²,

Shen³

et al. 2017

Pol. J. Food Nutr. Sci.

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Key words: ethanol extracts of Osmanthus fragrans fl owers, antioxidant, polyphenol profi les, cultured endothelial cells This study evaluated the antioxidant activity of ethanol extracts of Osmanthus fragrans (Thunb.) Lour. fl owers (EOF) and identifi ed phenolic compounds in EOF using liquid chromatography-mass spectrometry. Nine compounds, 3-O-caffeoylquinic acid, caffeic acid 4-O-glucoside, salidroside, 5-O-coumaroylquinic acid, 4-O-coumaroylquinic acid, acteoside, ligustroside, fucosterol and arjunolic acid were identifi ed. To our knowledge, caffeic acid 4-O-glucoside, 5-O-coumaroylquinic acid and 4-O-coumaroylquinic acid have not been detected in EOF. In vitro antioxidant activity analysis demonstrated that EOF possessed strong DPPH and ABTS radicals scavenging activity with EC 50 values at 0.26±0.06 mg/mL and 0.36±0.01 mg/mL, respectively, and reducing power with Ab 0.5 value at 13.04±0.16 μg/mL. The value of oxygen radical absorbance capacity (ORAC) was 333.23±13.39 μmol Trolox/g. Antioxidant activity assay in human umbilical vein endothelial cells (HUVEC) showed that the activity of superoxide dismutase (SOD) was signifi cantly improved and the reactive oxygen species (ROS) was removed effectively from cells when treated with EOF of 300~3000 μg/L.

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Section: Removal Of Rossupporting

confidence: 82%

Polyphenol Profiles and Antioxidant Properties of Ethanol Extracts from Osmanthus Fragrans (Thunb.) Lour. Flowers

Li¹,

Chai²,

Shen³

et al. 2017

Pol. J. Food Nutr. Sci.

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“…The same study reported that sodium orthovanadate, a protein phosphatase inhibitor, also reduced TNF-induced VCAM-1 expression while it further aggravated upregulation of ICAM-1. Similarly, genipin (a modulator of peroxisome proliferator-activated receptor γ) has been shown to suppress TNF-induced VCAM-1 but not ICAM-1 expression via alteration of Akt and protein kinase C pathways [57]. Recently published work from our group has demonstrated that inhibition of neuronal nitric oxide synthase aggravates TNF-mediated upregulation of ICAM-1 and various pro-inflammatory cytokines, while levels of VCAM-1 and the anti-inflammatory cytokine IL-10 remain unaltered [58].…”

Section: Discussionmentioning

confidence: 99%

Estradiol Modulates Tumor Necrosis Factor-Induced Endothelial Inflammation: Role of Tumor Necrosis Factor Receptor 2

Chakrabarti¹,

Davidge²

2012

J Vasc Res

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The sex hormone estradiol (E₂) appears to mediate both anti-atherogenic and pro-inflammatory effects in premenopausal women, suggesting a complex immunomodulatory role. Tumor necrosis factor (TNF) is a key pro-inflammatory cytokine involved in the pathogenesis of atherosclerosis and other inflammatory diseases. Alterations at the TNF receptors (TNFRs) and their downstream signaling/transcriptional pathways can affect inflammatory responses. Given this background, we hypothesized that chronic E₂ exposure would alter endothelial inflammatory response involving modulation at the levels of TNFRs and signaling pathways. HUVECs were used as the model system. Pre-treatment with E₂ did not significantly alter TNF-induced upregulation of pro-inflammatory molecules ICAM-1 (3–6 times) and VCAM-1 (5–7 times). However, pharmacological inhibition of transcriptional pathways suggested a partial shift from NF-ĸB (from 97 to 64%) towards the JNK/AP-1 pathway in ICAM-1 upregulation on E₂ treatment. In contrast, VCAM-1 expression remained NF-ĸB dependent in both control (∼96%) and E₂ treated (∼85%) cells. The pro-inflammatory TNF effects were mediated by TNFR1. Interestingly, E₂ pre-treatment increased TNFR2 levels in these cells. Concomitant TNFR2 activation (but not TNFR1 activation alone) led to the shift towards JNK/AP-1-mediated ICAM-1 upregulation in E₂-treated cells, suggesting the effects of chronic E₂ to be dependent on TNFR2 signaling.

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“…In one study, the plant alkaloid berberine was thought to increase atherosclerosis in ApoE null mice by supression of macrophage PTEN causing an increase in the expression of scavenger receptor SR-A, uptake of modified LDL, and foam cell formation (1027). Conversely, upregulation of PTEN in endothelial cells, either by specific alkaloids (810,1816) or by PPAR␥ agonists (810,838,909) substantially attenuated expression of the adhesion molecule VCAM-1 in response to the inflammatory cytokine TNF-␣ and decreased monocyte adherence while inhibiting endothelial proliferation and angiogenesis. These findings suggest a complex and difficult to predict role for PTEN in relation to atherogenesis.…”

Section: Signaling Cassettes Activated By Rtk Are Mutually Supportivementioning

confidence: 99%

Molecular Biology of Atherosclerosis

Hopkins

2013

Physiological Reviews

371

344

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At least 468 individual genes have been manipulated by molecular methods to study their effects on the initiation, promotion, and progression of atherosclerosis. Most clinicians and many investigators, even in related disciplines, find many of these genes and the related pathways entirely foreign. Medical schools generally do not attempt to incorporate the relevant molecular biology into their curriculum. A number of key signaling pathways are highly relevant to atherogenesis and are presented to provide a context for the gene manipulations summarized herein. The pathways include the following: the insulin receptor (and other receptor tyrosine kinases); Ras and MAPK activation; TNF-␣ and related family members leading to activation of NF-B; effects of reactive oxygen species (ROS) on signaling; endothelial adaptations to flow including G protein-coupled receptor (GPCR) and integrin-related signaling; activation of endothelial and other cells by modified lipoproteins; purinergic signaling; control of leukocyte adhesion to endothelium, migration, and further activation; foam cell formation; and macrophage and vascular smooth muscle cell signaling related to proliferation, efferocytosis, and apoptosis. This review is intended primarily as an introduction to these key signaling pathways. They have become the focus of modern atherosclerosis research and will undoubtedly provide a rich resource for future innovation toward intervention and prevention of the number one cause of death in the modern world.

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Genipin Selectively Inhibits TNF-α-activated VCAM-1 But Not ICAM-1 Expression by Upregulation of PPAR-γ in Human Endothelial Cells

Cited by 25 publications

References 20 publications

Polyphenol Profiles and Antioxidant Properties of Ethanol Extracts from Osmanthus Fragrans (Thunb.) Lour. Flowers

Polyphenol Profiles and Antioxidant Properties of Ethanol Extracts from Osmanthus Fragrans (Thunb.) Lour. Flowers

Estradiol Modulates Tumor Necrosis Factor-Induced Endothelial Inflammation: Role of Tumor Necrosis Factor Receptor 2

Molecular Biology of Atherosclerosis

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