PAF-Acether Induced Arterial Thrombosis and the Effect of Specific Antagonists

Bourgain, R.H.; Andries, R.; Esanu, André; Braquet, P.

doi:10.1007/978-1-4615-3404-4_48

Cited by 5 publications

(3 citation statements)

References 7 publications

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“…The anti-inflammatory effects of terpenoids due to inhibiting platelet activation factor are well established [4,5]. Comparative studies on cell-protective action by terpenes and flavones from G. biloba showed that ginkgolides and bilobalides do not appear to be responsi ble for antiradical and antilipoperoxidant ef fects in experimental models [ 12], In prelimi nary experiments (data not shown) we found proliferative effects of crude Ginkgo extract on fibroblast cultures not previously ob served.…”

Section: Discussionmentioning

confidence: 58%

“…Extracts from Ginkgo biloba leaves have anti-inflammatory, immunomodulatory and antioxidant properties and are now being clin ically studied in various pathologic conditions including cutaneous [1][2][3], cardiovascular [4,5], neurological [6,7], endocrinological [8] unique terpenoids and flavonoids, so-called ginkgoflavonoids, influence the normal func tion of fibroblasts. We here define the direct effect of Ginkgo extracts on normal human skin fibroblast.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Flavonoids of <i>Ginkgo biloba </i>on Proliferation of Human Skin Fibroblast

Kim

Mihye

Chun

et al. 1997

Skin Pharmacol Physiol

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Ginkgo bilobα studies have focused on the anti-inflammatory effects of the major components, ginkgolide and bilobalide, whereas little is known about their effect on fibroblasts. This study demonstrated the enhancing effects of Ginkgo L. extracts, especially the fiavonoid fractions: quercetin, kaempfe-rol, sciadopitysin, ginkgetin, isoginkgetin, on the proliferation of normal human skin fibroblast in vitro measured by MTT (3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyl-tetrazolium bromide) assay and direct hemocytometer cell count. Furthermore, increased production of collagen and extracellular fi-bronectin were documented by radioisotope (2,3-³H-proline) incorporated collagen assay, procollagen type I C-peptide assay and by immunoturbidimetric assay. These proliferative effects suggest another useful pharmacologic application of Ginkgo L. extracts in addition to their well-known anti-inflammatory effect.

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Section: Discussionmentioning

confidence: 58%

Section: Introductionmentioning

confidence: 99%

Effects of Flavonoids of <i>Ginkgo biloba </i>on Proliferation of Human Skin Fibroblast

Kim

Mihye

Chun

et al. 1997

Skin Pharmacol Physiol

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“…Gb has been shown to protect against Aβ-induced neurotoxicity [32, 33]. In addition, Gb showed anti-inflammatory activity through the antagonism of PAF [34, 35]. Among the constituents of terpene trilactones, ginkgolides A, B, and C are highly selective and competitive PAFR antagonists [33].…”

Section: Introductionmentioning

confidence: 99%

YY-1224, a terpene trilactone-strengthened Ginkgo biloba, attenuates neurodegenerative changes induced by β-amyloid (1-42) or double transgenic overexpression of APP and PS1 via inhibition of cyclooxygenase-2

Chung

Shin

et al. 2017

J Neuroinflammation

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Background Ginkgo biloba has been reported to possess free radical-scavenging antioxidant activity and anti-inflammatory properties. In our pilot study, YY-1224, a terpene trilactone-strengthened extract of G. biloba, showed anti-inflammatory, neurotrophic, and antioxidant effects.ResultsWe investigated the pharmacological potential of YY-1224 in β-amyloid (Aβ) (1-42)-induced memory impairment using cyclooxygenase-2 (COX-2) knockout (−/−) and APPswe/PS1dE9 transgenic (APP/PS1 Tg) mice. Repeated treatment with YY-1224 significantly attenuated Aβ (1-42)-induced memory impairment in COX-2 (+/+) mice, but not in COX-2 (−/−) mice. YY-1224 significantly attenuated Aβ (1-42)-induced upregulation of platelet-activating factor (PAF) receptor gene expression, reactive oxygen species, and pro-inflammatory factors. In addition, YY-1224 significantly inhibited Aβ (1-42)-induced downregulation of PAF-acetylhydrolase-1 (PAF-AH-1) and peroxisome proliferator-activated receptor γ (PPARγ) gene expression. These changes were more pronounced in COX-2 (+/+) mice than in COX-2 (−/−) mice. YY-1224 significantly attenuated learning impairment, Aβ deposition, and pro-inflammatory microglial activation in APP/PS1 Tg mice, whereas it significantly enhanced PAF-AH and PPARγ expression. A preferential COX-2 inhibitor, meloxicam, did not affect the pharmacological activity by YY-1224, suggesting that the COX-2 gene is a critical mediator of the neuroprotective effects of YY-1224. The protective activity of YY-1224 appeared to be more efficacious than a standard G. biloba extract (Gb) against Aβ insult.ConclusionsOur results suggest that the protective effects of YY-1224 against Aβ toxicity may be associated with its PAF antagonistic- and PPARγ agonistic-potential as well as inhibition of the Aβ-mediated pro-inflammatory switch of microglia phenotypes through suppression of COX-2 expression.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-017-0866-x) contains supplementary material, which is available to authorized users.

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YY162 prevents ADHD-like behavioral side effects and cytotoxicity induced by Aroclor1254 via interactive signaling between antioxidant potential, BDNF/TrkB, DAT and NET

Nam

Shin

et al. 2014

Food and Chemical Toxicology

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PAF-Acether Induced Arterial Thrombosis and the Effect of Specific Antagonists

Cited by 5 publications

References 7 publications

Effects of Flavonoids of <i>Ginkgo biloba </i>on Proliferation of Human Skin Fibroblast

Effects of Flavonoids of <i>Ginkgo biloba </i>on Proliferation of Human Skin Fibroblast

YY-1224, a terpene trilactone-strengthened Ginkgo biloba, attenuates neurodegenerative changes induced by β-amyloid (1-42) or double transgenic overexpression of APP and PS1 via inhibition of cyclooxygenase-2

YY162 prevents ADHD-like behavioral side effects and cytotoxicity induced by Aroclor1254 via interactive signaling between antioxidant potential, BDNF/TrkB, DAT and NET

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