Shoji N, Oshika T, Masuda K
Department of Ophthalmology, Musashino Red Cross Hospital, Tokyo, Japan.
Nippon Ganka Gakkai Zasshi. 1997 Apr;101(4):305-11.
To assess the receptors which mediate the inflammatory reaction induced by endothelin-1 (ET-1), we investigated the influence of pre-treatment with an ETA receptor antagonist (97-139) on the increase of aqueous protein concentration (APC) after the injection of ET-1 (10(-4), 10(-5)M) into the vitreous cavity of pigmented rabbits. The concentration of prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) in the aqueous humor after the injection of 10(-4)M ET-1 with or without pre-treatment with 97-139 (10(-1), 10(-2), 10(-3)M) was also studied. Pre-treatment with 10(-2)M and 10(-1)M 97-139 completely prevented the APC increase induced by 10(-5)M and 10(-4)M ET-1, respectively. Increases in aqueous PGE2 concentration were observed after the injection of ET-1, which was inhibited by pre-treatment with 97-139. Aqueous LTB4 concentration was not changed significantly by ET-1. These results indicate that the effects of ET-1 on APC are at least partially mediated by the cyclooxygenase pathway of arachidonic acid cascade, and that ETA receptors play an important role in these reactions.
为了评估介导内皮素 -1（ET-1）诱导的炎症反应的受体，我们研究了用 ETA 受体拮抗剂（97 - 139）预处理对向有色家兔玻璃体腔注射 ET-1（10⁻⁴、10⁻⁵M）后房水蛋白浓度（APC）升高的影响。还研究了在注射 10⁻⁴M ET-1 时，无论是否用 97 - 139（10⁻¹、10⁻²、10⁻³M）预处理，房水中前列腺素 E2（PGE2）和白三烯 B4（LTB4）的浓度。用 10⁻²M 和 10⁻¹M 97 - 139 预处理分别完全阻止了由 10⁻⁵M 和 10⁻⁴M ET-1 诱导的 APC 升高。注射 ET-1 后观察到房水 PGE2 浓度升高，这被 97 - 139 预处理所抑制。ET-1 对房水 LTB4 浓度无明显影响。这些结果表明，ET-1 对 APC 的作用至少部分是由花生四烯酸级联的环氧化酶途径介导的，并且 ETA 受体在这些反应中起重要作用。
