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玻璃体内注射内皮素-1后通过花生四烯酸级联反应引发的炎症反应。

Inflammatory reaction via arachidonic acid cascade after intravitreal injection of endothelin-1.

作者信息

Shoji N, Oshika T, Masuda K

机构信息

Department of Ophthalmology, Musashino Red Cross Hospital, Tokyo, Japan.

出版信息

Curr Eye Res. 1998 Feb;17(2):205-10. doi: 10.1076/ceyr.17.2.205.5612.

Abstract

PURPOSE

To investigate the characteristics of anterior chamber inflammatory reaction induced by intravitreal injection of endothelin-1 (ET-1).

METHODS

The time course of changes in aqueous protein concentration (APC) after intravitreal injection of 10(-4), 10(-5), 10(-6) and 10(-7) M ET-1 into rabbit eyes was measured with a laser flare-cell meter. The influence of a topical diclofenac sodium (DFNa) pre- and post-treatment was assessed. Aqueous prostaglandin E2 and leukotriene B4 concentration was quantified using a radioimmunoassay technique.

RESULTS

Intravitreal injection of 10(-4) and 10(-5) M ET-1 significantly increased APC, while 10(-6) and 10(-7) M ET-1 did not induce anterior chamber inflammation. After 10(-5) M ET-1 injection, APC reached a maximum at 4 h post-treatment and returned to a normal level 48 h after injection. Eyes treated with 10(-4) M ET-1 displayed a bi-phasic time course, with peak values observed 4 to 8 h as well as 48 h after administration. Pre- and post-treatment with topical DFNa completely suppressed the APC increase in the 10(-5) M ET-1 preparation, and considerably inhibited it in the 10(-4) M ET-1 preparation. After ET-1 injection, aqueous prostaglandin E2 concentration increased significantly, followed by an increase in APC. There were no changes in leukotriene B4 concentration.

CONCLUSIONS

ET-1 induces anterior chamber inflammation via the cyclooxygenase pathway of the arachidonic acid cascade. The lipoxygenase pathway is not involved in this reaction.

摘要

目的

研究玻璃体内注射内皮素-1(ET-1)诱导的前房炎症反应特征。

方法

用激光散射细胞仪测量向兔眼玻璃体内注射10⁻⁴、10⁻⁵、10⁻⁶和10⁻⁷M ET-1后房水蛋白浓度(APC)的变化时间进程。评估局部应用双氯芬酸钠(DFNa)预处理和后处理的影响。采用放射免疫分析技术定量房水前列腺素E2和白三烯B4浓度。

结果

玻璃体内注射10⁻⁴和10⁻⁵M ET-1可显著增加APC,而10⁻⁶和10⁻⁷M ET-1未诱导前房炎症。注射10⁻⁵M ET-1后,APC在治疗后4小时达到最大值,并在注射后48小时恢复到正常水平。用10⁻⁴M ET-1治疗的眼睛显示出双相时间进程,在给药后4至8小时以及48小时观察到峰值。局部DFNa预处理和后处理完全抑制了10⁻⁵M ET-1制剂中APC的增加,并在10⁻⁴M ET-1制剂中显著抑制了APC的增加。注射ET-1后,房水前列腺素E2浓度显著增加,随后APC增加。白三烯B4浓度无变化。

结论

ET-1通过花生四烯酸级联反应的环氧化酶途径诱导前房炎症。脂氧化酶途径不参与此反应。

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