Denko C W
Pharmacology. 1974;12(6):331-9. doi: 10.1159/000136556.
By use of two novel techniques for detecting extremely small amounts of PGs, studies were conducted elucidating the mechanism of urate crystal-induced inflammation. Rats deficient in EFA and thus deficient in PGs received injections of monosodium urate crystals into the footpad. The EFA-deficient animals developed less swelling than did normal animals. However, when a 1-ng dose of PGE-1, PGE-2, PGA-2, or PGF-2-alpha was added along with the urate injection the swelling was enhanced to approximately normal levels. In the second technique the swelling induced by injection of two different urate crystals was compared. Urate crystals heated to 200 degrees C produced less swelling in normal rats than did similar urate crystals heated only to 50 degrees C. However when a 1-ng dose of PGE-1, PGE-2 or PGF-2-alpha was added to the heated urate crystals injection the swelling increased to approximately the swelling in normal controls receiving urate heated to 50 degrees C. Comments are presented suggesting that urate crystal inflammation may be a membrane disease.
通过使用两种检测极少量前列腺素(PGs)的新技术,开展了相关研究以阐明尿酸盐晶体诱导炎症的机制。缺乏必需脂肪酸(EFA)从而缺乏PGs的大鼠,其足垫被注射尿酸单钠晶体。与正常动物相比,缺乏EFA的动物肿胀程度较轻。然而,当在注射尿酸盐的同时加入1纳克剂量的前列腺素E-1(PGE-1)、前列腺素E-2(PGE-2)、前列腺素A-2(PGA-2)或前列腺素F-2α(PGF-2-α)时,肿胀程度增强至大致正常水平。在第二种技术中,比较了注射两种不同尿酸盐晶体所诱导的肿胀情况。加热至200摄氏度的尿酸盐晶体在正常大鼠中引起的肿胀比仅加热至50摄氏度的类似尿酸盐晶体要小。然而,当在加热的尿酸盐晶体注射中加入1纳克剂量的PGE-1、PGE-2或PGF-2-α时,肿胀增加至大致与接受加热至50摄氏度尿酸盐的正常对照组的肿胀程度相同。文中提出观点,认为尿酸盐晶体炎症可能是一种膜疾病。