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真皮来源的15-羟基二十碳四烯酸抑制表皮12-脂氧合酶活性。

Dermis-derived 15-hydroxy-eicosatetraenoic acid inhibits epidermal 12-lipoxygenase activity.

作者信息

Kragballe K, Pinnamaneni G, Desjarlais L, Duell E A, Voorhees J J

出版信息

J Invest Dermatol. 1986 Oct;87(4):494-8. doi: 10.1111/1523-1747.ep12455564.

DOI:10.1111/1523-1747.ep12455564
PMID:3093592
Abstract

The purpose of the present study was to analyze the metabolism of arachidonic acid (AA) in normal human dermis. After incubating homogenized dermis with exogenous AA, the extracted lipids were isolated by reversed-phase high-performance liquid chromatography. Each chromatographic peak was characterized by its UV absorption spectrum and identified by its coelution with the appropriate authentic standard and by radioimmunoassay of its eluate fraction. Identified compounds were quantitated by integrated optical density. Homogenized human dermis transformed AA into both cyclooxygenase and lipoxygenase products, but predominantly 15-hydroxy-eicosatetraenoic acid (15-HETE). Cultured fibroblasts from normal human dermis also mainly metabolized AA into 15-HETE. To determine whether dermis-derived 15-HETE might modify the AA metabolism of epidermis, normal human epidermis was incubated with dermis. Increasing amounts of dermis resulted in an increasing inhibition of epidermal 12-HETE formation. Similarly, 15-HETE alone induced a dose-dependent decrease of epidermal 12-HETE formation, while the formation of prostaglandin E2 was unchanged. Since 12-HETE possess the ability to elicit skin inflammation and to stimulate epidermal DNA synthesis, 15-HETE formation may be a way whereby dermis regulates important epidermal activities.

摘要

本研究的目的是分析正常人真皮中花生四烯酸(AA)的代谢情况。用外源性AA孵育匀浆真皮后,通过反相高效液相色谱法分离提取的脂质。每个色谱峰通过其紫外吸收光谱进行表征,并通过与适当的标准品共洗脱及其洗脱级分的放射免疫测定进行鉴定。鉴定出的化合物通过积分光密度进行定量。匀浆的人真皮将AA转化为环氧化酶和脂氧化酶产物,但主要是15-羟基-二十碳四烯酸(15-HETE)。正常人真皮培养的成纤维细胞也主要将AA代谢为15-HETE。为了确定真皮来源的15-HETE是否可能改变表皮的AA代谢,将正常人表皮与真皮一起孵育。真皮量的增加导致表皮12-HETE形成的抑制增加。同样,单独的15-HETE诱导表皮12-HETE形成呈剂量依赖性降低,而前列腺素E2的形成不变。由于12-HETE具有引发皮肤炎症和刺激表皮DNA合成的能力,15-HETE的形成可能是真皮调节重要表皮活动的一种方式。

相似文献

1
Dermis-derived 15-hydroxy-eicosatetraenoic acid inhibits epidermal 12-lipoxygenase activity.真皮来源的15-羟基二十碳四烯酸抑制表皮12-脂氧合酶活性。
J Invest Dermatol. 1986 Oct;87(4):494-8. doi: 10.1111/1523-1747.ep12455564.
2
In vitro synthesis of 12-hydroxy-eicosatetraenoic acid is increased in uninvolved psoriatic epidermis.未受累银屑病表皮中12-羟基-二十碳四烯酸的体外合成增加。
J Invest Dermatol. 1986 Jul;87(1):47-52. doi: 10.1111/1523-1747.ep12523561.
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Selective decrease of 15-hydroxyeicosatetraenoic acid (15-HETE) formation in uninvolved psoriatic dermis.银屑病未受累真皮中15-羟基二十碳四烯酸(15-HETE)生成的选择性降低。
Arch Dermatol. 1986 Aug;122(8):877-80.
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In vitro inhibition of leukotriene B4 formation by exogeneous 5-lipoxygenase inhibitors is associated with enhanced generation of 15-hydroxy-eicosatetraenoic acid (15-HETE) by human neutrophils.外源性5-脂氧合酶抑制剂对白细胞三烯B4形成的体外抑制作用与人中性粒细胞生成15-羟基-二十碳四烯酸(15-HETE)的增加有关。
Arch Dermatol Res. 1988;280(7):430-6. doi: 10.1007/BF00429983.
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Endogenous hydroxyeicosatetraenoic acids stimulate the human polymorphonuclear leukocyte 15-lipoxygenase pathway.内源性羟基二十碳四烯酸刺激人类多形核白细胞15-脂氧合酶途径。
J Biol Chem. 1985 Dec 15;260(29):15482-7.
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Biosynthesis of lipoxygenase products by enzyme preparations from normal and psoriatic skin.来自正常皮肤和银屑病皮肤的酶制剂对脂氧合酶产物的生物合成
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Lipoxygenase pathway in islet endocrine cells. Oxidative metabolism of arachidonic acid promotes insulin release.胰岛内分泌细胞中的脂氧合酶途径。花生四烯酸的氧化代谢促进胰岛素释放。
J Clin Invest. 1983 May;71(5):1191-205. doi: 10.1172/jci110868.
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An enzymatic method for distinguishing the stereoisomers of 12-hydroxyeicosatetraenoic acid in human epidermis and psoriatic scale.一种区分人表皮和银屑病鳞屑中12-羟基二十碳四烯酸立体异构体的酶法。
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Metabolism of arachidonic acid by human epidermal cells depends upon maturational stage.人表皮细胞对花生四烯酸的代谢取决于成熟阶段。
J Invest Dermatol. 1991 Aug;97(2):291-7. doi: 10.1111/1523-1747.ep12480558.
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Effects of hydroxyeicosatetraenoic acids on fatty acid esterification in phospholipids and insulin secretion in pancreatic islets.羟基二十碳四烯酸对磷脂中脂肪酸酯化及胰岛胰岛素分泌的影响。
Endocrinology. 1985 Sep;117(3):1011-9. doi: 10.1210/endo-117-3-1011.

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