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前列腺素在补骨脂素加紫外线A诱导的炎症中可能发挥的作用:来自器官培养皮肤的启示

A possible role of prostaglandins in PUVA-induced inflammation: implication by organ cultured skin.

作者信息

Imokawa G, Tejima T

机构信息

Tochigi Research Laboratories, Kao Corporation, Japan.

出版信息

J Invest Dermatol. 1989 Feb;92(2):296-300. doi: 10.1111/1523-1747.ep12276882.

Abstract

The role of arachidonate metabolites in UV-induced inflammation was analyzed by measuring the amounts of prostaglandins or leukotrienes released into a culture medium in the organ culture of biopsied guinea pig skin following UV exposure. Increased concentrations of prostaglandin E2, F2 alpha, and 6-oxo-F1 alpha were found in the medium subjected to UVB radiation followed by 24 h incubation in the organ culture, compared to medium from non-exposed skin, whereas LTC4 was at an undetectable level in both. This release occurred in UVB dose-dependent fashion and was completely inhibited by the addition of indomethacin to the medium. Exposure to monochromatic UV light of 250, 300, and 350 nm released prostaglandin E2, F2 alpha, and 6-oxo-F1 alpha, in increasing order of 250, 300, and 350 nm, but not LTC4. This order of amount released almost paralleled the intensity of inflammation that occurred with each wavelength. Exposure of skin to UVA following intraperitoneal injection of 8-methoxypsoralen (PUVA) was also found to stimulate the synthesis of prostaglandin E2 in UVA dose-dependent fashion, and the stimulation through an increasing dose of UVA occurred more significantly than UVB exposure. The time course of prostaglandin release following UVB and PUVA exposures was found to have a pattern similar to their dynamics in association with erythema and edema, conditions which could be significantly diminished by the topical application of indomethacin. The present studies demonstrate that prostaglandins play an important role in the production of inflammation by UVB as well as UVA and PUVA.

摘要

通过测量紫外线照射后活检豚鼠皮肤器官培养物中释放到培养基中的前列腺素或白三烯的量,分析了花生四烯酸代谢产物在紫外线诱导的炎症中的作用。与未暴露皮肤的培养基相比,经UVB辐射后在器官培养中孵育24小时的培养基中,前列腺素E2、F2α和6-氧代-F1α的浓度升高,而两者中的LTC4均处于无法检测的水平。这种释放以UVB剂量依赖性方式发生,并且通过向培养基中添加吲哚美辛而被完全抑制。暴露于250、300和350nm的单色紫外线会释放前列腺素E2、F2α和6-氧代-F1α,其释放顺序为250、300和350nm递增,但不会释放LTC4。这种释放量的顺序几乎与每个波长发生的炎症强度平行。还发现腹腔注射8-甲氧基补骨脂素(PUVA)后皮肤暴露于UVA会以UVA剂量依赖性方式刺激前列腺素E2的合成,并且通过增加UVA剂量的刺激比UVB暴露更显著。发现UVB和PUVA暴露后前列腺素释放的时间进程具有与其在红斑和水肿相关的动力学相似的模式,局部应用吲哚美辛可显著减轻这些症状。本研究表明,前列腺素在UVB以及UVA和PUVA诱导的炎症产生中起重要作用。

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