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糖皮质激素诱导的胃黏膜损伤:对白三烯生物合成的抑制作用,而非前列腺素生物合成。

Glucocorticoid-induced gastric mucosal damage: inhibition of leukotriene, but not prostaglandin biosynthesis.

作者信息

Wallace J L

机构信息

Department of Physiology, Queen's University, Kingston, Ontario, Canada.

出版信息

Prostaglandins. 1987 Aug;34(2):311-23. doi: 10.1016/0090-6980(87)90252-8.

DOI:10.1016/0090-6980(87)90252-8
PMID:2823319
Abstract

The effects of daily administration of ulcerogenic doses of the glucocorticoids, dexamethasone and prednisolone, on gastric prostaglandin and leukotriene synthesis were examined in the rat. Significant gastric damage was not observed until the fourth day of treatment with dexamethasone and until the sixth day of treatment with prednisolone. However, the onset of gastric damage was not accompanied by any significant effect of these drugs on gastric 6-keto prostaglandin Fl alpha synthesis. Conversely, both drugs caused a reduction in gastric leukotriene C4 synthesis, with dexamethasone producing a highly significant (p less than 0.001) effect. Furthermore, there was a highly significant (p less than 0.001) correlation between the ability of these drugs to inhibit gastric leukotriene C4 synthesis, and their ability to reduce gastric tissue levels of the neutrophilic enzyme myeloperoxidase. Thus, glucocorticoid-induced gastric damage does not appear to be related to inhibitory effects of these drugs on prostaglandin synthesis. Whether or not effects of these drugs on gastric leukotriene C4 synthesis and myeloperoxidase activity are relevant to the mechanism of ulceration is unclear.

摘要

在大鼠中研究了每日给予致溃疡剂量的糖皮质激素地塞米松和泼尼松龙对胃前列腺素和白三烯合成的影响。在用 地塞米松治疗的第 4 天之前和用泼尼松龙治疗的第 6 天之前均未观察到明显的胃损伤。然而,胃损伤的发生并未伴随这些药物对胃 6-酮前列腺素 F1α 合成产生任何显著影响。相反,两种药物均导致胃白三烯 C4 合成减少,地塞米松产生了高度显著(p < 0.001)的效果。此外,这些药物抑制胃白三烯 C4 合成的能力与其降低胃组织中嗜中性粒细胞酶髓过氧化物酶水平的能力之间存在高度显著(p < 0.001)的相关性。因此,糖皮质激素诱导的胃损伤似乎与这些药物对前列腺素合成的抑制作用无关。这些药物对胃白三烯 C4 合成和髓过氧化物酶活性的影响是否与溃疡形成机制相关尚不清楚。

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