Teitz C C, Chrisman O D
Clin Orthop Relat Res. 1975 May(108):264-74. doi: 10.1097/00003086-197505000-00039.
Prostaglandins are found in increased concentrations in various arthritic joint fluids, and the E and F series have been shown to produce inflammation. Vane suggests that the effectiveness of aspirin is mediated by inhibition of synthesis or release of prostaglandins. In our studies PGE-1 intra-articularly produced the greatest amount of synovial and cartilage damage of the several PGs tested. Five knee intra-articular injections of 500 ng PGE-1 were given to 12 mature white New Zealand rabbits at 4 day intervals, with control solutions on the opposite sides. Four with intramuscular chloroquine at clinical levels and 4 controls. At 20 days histologic examination with H & E and safranin-O showed increased synovitis and abnormal cartilage in the controls and salicylate groups, normal cartilage in the chloroquine group. Whereas chloroquine's ability to stabilize cell membranes is protective in this experiment, salicylate's ability to prevent biosynthesis of prostaglandins is bypassed and therefore is not protective. Vane's hypothesis is supported by this study of PG induced experimental arthritis.
前列腺素在各种关节炎关节液中的浓度升高,并且已证明E系列和F系列会引发炎症。万恩认为阿司匹林的有效性是通过抑制前列腺素的合成或释放来介导的。在我们的研究中,在所测试的几种前列腺素中,关节内注射前列腺素E-1(PGE-1)造成的滑膜和软骨损伤量最大。给12只成熟的新西兰白兔每隔4天膝关节内注射500纳克PGE-1,共注射5次,另一侧注射对照溶液。4只注射临床剂量的肌肉注射氯喹,4只为对照。20天时,用苏木精和伊红(H&E)以及番红O进行组织学检查,结果显示对照组和水杨酸盐组滑膜炎加重且软骨异常,氯喹组软骨正常。在该实验中,氯喹稳定细胞膜的能力具有保护作用,而水杨酸盐防止前列腺素生物合成的能力则被绕过,因此没有保护作用。对前列腺素诱导的实验性关节炎的这项研究支持了万恩的假说。