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非甾体抗炎药的COX-2抑制、细胞凋亡与化学预防

COX-2 inhibition, apoptosis, and chemoprevention by nonsteroidal anti-inflammatory drugs.

作者信息

Moore B C, Simmons D L

机构信息

Department of Chemistry and Biochemistry, Brigham Young University, Provo, Utah 84602, USA.

出版信息

Curr Med Chem. 2000 Nov;7(11):1131-44. doi: 10.2174/0929867003374273.

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) have as their common mechanism the inhibition of cyclooxygenase (COX) enzymes, of which two isoforms (COX-1 and COX-2) exist. The effect of NSAIDs on chemoprevention and tumor regression has been shown in animal models, epidemiologic studies, and in treatment of patients. The exact biochemical and cellular mechanisms underlying each of these phenomena is only partially understood. Processes that have been recently implicated as being important include the inhibition of tumor cell growth, prevention of angiogenesis, and induction of apoptosis in neoplastic cells.

摘要

非甾体抗炎药(NSAIDs)的共同作用机制是抑制环氧化酶(COX),该酶存在两种同工型(COX - 1和COX - 2)。NSAIDs在化学预防和肿瘤消退方面的作用已在动物模型、流行病学研究及患者治疗中得到证实。对于这些现象背后确切的生化和细胞机制,目前仅了解一部分。最近认为重要的过程包括抑制肿瘤细胞生长、预防血管生成以及诱导肿瘤细胞凋亡。

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