Vitamin E inhibits PGE2 and O2− production in rat peritoneal macrophages

Sakamoto, Wataru; Fujie, Katsutoshi; Handa, Hiroshi; Nishihira, Jun; Mino, Makoto

doi:10.1016/0304-4165(91)90160-i

Cited by 25 publications

(10 citation statements)

References 16 publications

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“…These findings suggest that a possible role of vitamin E may be an inhibitor of cell membrane-modulation. This is compatible with the report that vitamin E inhibits 02-production from activated macrophages, probably through an interaction with membrane lipids (13). In addition, Kamimura (14) suggested that vitamin E has an effect on mast cell membrane-modulation during development of skin irritations caused by applications of croton oil and plaster.…”

Section: Discussionsupporting

confidence: 90%

Effect of Vitamin E on Keratinocyte-Modulation Induced by Lauroylsarcosine

Shimizu

Aioi

Horiguchi

et al. 1995

Japanese Journal of Pharmacology

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ABSTRACT-The effect of vitamin E on the modulation of keratinocytes was studied in rats. A 1°10 lauroylsarcosine (LS) ointment caused skin erythema with keratinocyte-damage. A 30% vitamin E ointment markedly alleviated this erythema and protected keratinocytes from cell damage. Vitamin E (100 pg/ml) was also effective on LS (7.5 pg/ml)-induced proliferative reduction of cultured keratinocytes. On the other hand, ointment containing superoxide dismutase (SOD) (99,000 U/g) decreased the LS-induced erythema, suggesting that superoxide anion (02) produced from keratinocytes play an important role in the skin irritation. Indeed, LS induced 02-production from cultured keratinocytes. The 02-was significantly reduced by vitamin E and SOD, although vitamin E had no effects on 02-production in a xanthine-xanthine oxidase system, unlike the effect observed with SOD. These results indicate that vitamin E is an inhibitor of keratinocyte-modulation.

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Section: Discussionsupporting

confidence: 90%

Effect of Vitamin E on Keratinocyte-Modulation Induced by Lauroylsarcosine

Shimizu

Aioi

Horiguchi

et al. 1995

Japanese Journal of Pharmacology

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“…66 However, in the present report, AT had no significant effect on PGE 2 levels from LPS-activated monocytes. Our findings are supported by the work of Sakamoto et al, 65 who also showed that AT failed to inhibit PGE 2 production in LPS-stimulated rat macrophages. In addition, we show that indomethacin, a COX inhibitor, although significantly decreasing PGE 2 levels in LPS-activated monocytes, did not produce any significant increase in IL-1␤ release from activated monocytes.…”

Section: Effect Of Mk886 At and Indomethacin On Il-1␤ Release From supporting

confidence: 82%

“…Correspondingly, nonsteroidal anti-inflammatory compounds that effectively suppress COX activity demonstrated a dosedependent augmentation of IL-1 release. 65 AT, in certain systems such as rat peritoneal and avian macrophages, has been shown to decrease COX activity and would thus be expected to increase IL-1␤ levels. 66 However, in the present report, AT had no significant effect on PGE 2 levels from LPS-activated monocytes.…”

Section: Effect Of Mk886 At and Indomethacin On Il-1␤ Release From mentioning

confidence: 99%

α-Tocopherol Decreases Interleukin-1β Release From Activated Human Monocytes by Inhibition of 5-Lipoxygenase

Devaraj

Jialal

1999

ATVB

143

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Abstract-Cardiovascular disease is the leading cause of morbidity and mortality in westernized populations. Low levels of ␣-tocopherol (AT) are associated with increased incidence of atherosclerosis and increased intakes appear to be protective. Recently, we showed that supplementation with AT resulted in significant decreases in monocyte superoxide anion release, lipid oxidation, interleukin-1␤ (IL-1␤) release, and adhesion to endothelium. The reduction in superoxide and lipid oxidation by AT seemed to be mediated by inhibition of protein kinase C. The aim of this study was to investigate the mechanism(s) by which AT inhibits IL-1␤ release. Potential mechanisms examined included its effect as an antioxidant and its inhibitory effects on protein kinase C and the cyclooxygenase-lipoxygenase pathways. Although AT decreased superoxide release from activated monocytes, superoxide dismutase and catalase had no effect on IL-1␤ release. Also, a similar antioxidant, ␤-tocopherol, had no effect on IL-1␤ release. The protein kinase C inhibitor, bisindolylmaleimide, did not inhibit IL-1␤ release from activated monocytes, in spite of AT decreasing protein kinase C activity. Leukotriene B 4 , a major product of 5-lipoxygenase, has been shown to augment IL-1␤ release. In the presence of AT, a significant reduction in leukotriene B 4 and IL-1␤ levels was observed, which was reversed by the addition of leukotriene B 4 . Similar observations were seen with specific inhibitors of 5-lipoxygenase. The product of cyclooxygenase, prostaglandin E 2 , has been shown to inhibit IL-1␤ activity in some systems. However, AT had no significant effect on prostaglandin E 2 levels in activated monocytes. In the presence of indomethacin, a cyclooxygenase inhibitor, AT inhibited IL-1␤ activity. Also, AT had no effect on IL-1␤ mRNA levels or stability, suggesting a posttranscriptional effect. Thus, in activated human monocytes, AT exerts a novel biological effect of inhibiting the release of the proinflammatory cytokine, IL-1␤, via inhibition of the 5-lipoxygenase pathway. Key Words: vitamin E Ⅲ cytokine Ⅲ interleukins Ⅲ protein kinase C Ⅲ leukotriene A lthough low levels of ␣-tocopherol (AT) are associated with increased risk for cardiovascular disease, increased intakes appear to be protective. [1][2][3][4][5][6] In addition to AT decreasing the oxidative susceptibility of LDL, 7-9 it could have effects on other crucial cells in atherogenesis, such as monocytes, that could prove beneficial. We previously showed that in vivo supplementation with AT significantly decreases monocyte superoxide anion release, lipid oxidation, interleukin-1␤ (IL-1␤) release, and adhesion to endothelial cells. 10 In that study it appeared that the inhibition of superoxide anion release and lipid oxidation was mediated by inhibition of protein kinase C (PKC) by AT. However, we did not investigate the mechanism(s) by which AT inhibits IL-1␤ release and monocyte-endothelial cell adhesion. Recently, we showed that AT enrichment of monocytes decreased agonist-induced adhe...

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“…suggested an alternative explanation to post-translational modulation of COX activity by vitamin E (Sakamoto et al , 1993). They reported that PGE2 production stimulated by phorbol 12-myristate 13-acetate or A-23187 was inhibited by intraperitoneal injection of vitamin E via suppression of phospholipase A2 (PLA2) activity and the subsequent decrease in arachidonic acid release (Sakamoto et al , 1991; Sakamoto et al , 1993). The latter mechanism may be relevant to our findings because we observed augmented PGE2 production with endogenous arachidonic acid in BDE-47-treated HTR-8/SVneo cells compared to controls without exogenous arachidonic acid supplementation (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of (±)α-tocopherol on brominated diphenyl ether-47-stimulated prostaglandin pathways in human extravillous trophoblasts in vitro

Park

Loch‐Caruso

2015

Toxicology in Vitro

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Brominated diphenyl ether (BDE)-47 is a prevalent flame retardant chemical found in human tissues and is linked to adverse pregnancy outcomes in humans. Because dysregulation of the prostaglandin pathway is implicated in adverse pregnancy outcomes, the present study investigates BDE-47 induction of prostaglandin synthesis in a human extravillous trophoblast cell line, HTR-8/SVneo, examining the hypothesis that BDE-47 increases generation of reactive oxygen species (ROS) to stimulate the prostaglandin response. Treatment with 20 μM BDE-47 significantly increased mRNA expression of prostaglandin-endoperoxide synthase 2 (PTGS2) at 4, 12 and 24 h, and 24-h treatment significantly increased cyclooxygenase (COX)-2 cellular protein expression and prostaglandin E2 (PGE2) concentration in culture medium. The BDE-47-stimulated PGE2 release was inhibited by the COX inhibitors indomethacin and NS398, implicating COX activity. Exposure to 20 μM BDE-47 significantly increased ROS generation as measured by carboxydichlorofluorescein fluorescence, and this response was blocked by cotreatment with the peroxyl radical scavenger (±)-α-tocopherol. (±)-α-Tocopherol cotreatment suppressed BDE-47-stimulated increases of PGE2 release without significant effects on COX-2 mRNA and protein expression, implicating a role for ROS in post-translational regulation of COX activity. Because prostaglandins regulate trophoblast functions necessary for placentation and pregnancy, further investigation is warranted of BDE-47 impacts on trophoblast responses.

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Vitamin E inhibits PGE2 and O2− production in rat peritoneal macrophages

Cited by 25 publications

References 16 publications

Effect of Vitamin E on Keratinocyte-Modulation Induced by Lauroylsarcosine

Effect of Vitamin E on Keratinocyte-Modulation Induced by Lauroylsarcosine

α-Tocopherol Decreases Interleukin-1β Release From Activated Human Monocytes by Inhibition of 5-Lipoxygenase

Protective effect of (±)α-tocopherol on brominated diphenyl ether-47-stimulated prostaglandin pathways in human extravillous trophoblasts in vitro

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