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阿司匹林诱导鸡胚神经管缺陷的机制。

Mechanism of aspirin induced neural tube defect in chick embryo.

作者信息

Kotwani A, Mehta V L, Iyengar B

机构信息

Department of Pharmacology, Maulana Azad Medical College, New Delhi.

出版信息

Indian J Med Res. 1994 Jun;99:289-94.

PMID:8088892
Abstract

The effect of acetyl salicylic acid (aspirin) on neural tube development in chick embryo was studied, using the chick embryo blastoderm model. Aspirin was injected in four different doses sub-blastodermally into fresh embryonated eggs. The role of PGE1 and PGE2 alpha in the defect induced by aspirin on neural tube development in chick embryo was studied. PGE1 (5 micrograms) given after aspirin (30 micrograms) treatment was found to produce greater defect in development. All the four doses of aspirin used (i.e., 6, 30, 60 and 120 micrograms/embryo) produced significant changes (P < 0.01) in the neural tube development of chick embryo. Pre-treatment with PGE1 did not modify the defect induced by aspirin, whereas pre-treatment with PGF2 alpha prevented neural tube defects induced by aspirin. It appears that aspirin (in the doses used) affects neural tube formation by decreasing PGF2 alpha synthesis in chick embryo blastoderm.

摘要

利用鸡胚胚盘模型研究了乙酰水杨酸(阿司匹林)对鸡胚神经管发育的影响。将阿司匹林以四种不同剂量经胚盘下注射到新鲜的受精鸡蛋中。研究了前列腺素E1(PGE1)和前列腺素E2α(PGE2α)在阿司匹林诱导的鸡胚神经管发育缺陷中的作用。发现在阿司匹林(30微克)处理后给予PGE1(5微克)会导致更大的发育缺陷。所用的所有四种剂量的阿司匹林(即6、30、60和120微克/胚胎)均使鸡胚神经管发育产生了显著变化(P<0.01)。PGE1预处理并未改变阿司匹林诱导的缺陷,而PGF2α预处理则预防了阿司匹林诱导的神经管缺陷。看来(所用剂量的)阿司匹林通过减少鸡胚胚盘中PGF2α的合成来影响神经管形成。

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