Kis Bela, Snipes James A, Busija David W
Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, NC 27157, USA.
J Pharmacol Exp Ther. 2005 Oct;315(1):1-7. doi: 10.1124/jpet.105.085431. Epub 2005 May 6.
Cyclooxygenase (COX)-3, a novel COX splice variant, was suggested as the key to unlocking the mystery of the mechanism of action of acetaminophen. Although COX-3 might have COX activity in canines, and this activity might be inhibited by acetaminophen, its low expression level and the kinetics indicate unlikely clinical relevance. In rodents and humans, COX-3 encodes proteins with completely different amino acid sequences than COX-1 or COX-2 and without COX activity; therefore, it is improbable that COX-3 in these species plays a role in prostaglandin-mediated fever and pain. The aim of this review is to evaluate the literature that seeks to point out critical theoretical and methodological limitations of the COX-3 studies that led several investigators to scientifically questionable conclusions.
环氧化酶（COX）-3是一种新型的COX剪接变体，被认为是解开对乙酰氨基酚作用机制之谜的关键。尽管COX-3在犬类中可能具有COX活性，且这种活性可能被对乙酰氨基酚抑制，但其低表达水平和动力学表明其临床相关性不大。在啮齿动物和人类中，COX-3编码的蛋白质氨基酸序列与COX-1或COX-2完全不同且无COX活性；因此，这些物种中的COX-3不太可能在前列腺素介导的发热和疼痛中发挥作用。本综述的目的是评估相关文献，这些文献旨在指出COX-3研究的关键理论和方法局限性，这些局限性导致一些研究人员得出了科学上有疑问的结论。
