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早在1988年一项流行病学研究报告发现,长期使用非甾体类抗炎药(nonsteroidal anti-inflammatory drugs,NSAIDs)可以抑制结肠癌的发生、发展[1];新近的研究证据表明环氧化酶2(COX-2)参与了肿瘤发生、发展中的许多生物学进程[2]。不同于以往的以核苷酸代谢为抗癌核心的理念,COX-2成为了肿瘤防治的新靶点。大量的流行病学和临床研究结果证实,COX-2及其催化产生的前列腺素产物与肿瘤的演变密切相关,选择性COX-2抑制剂可能阻碍着恶性肿瘤的发展[2]。
As early as 1988, an epidemiological study found that long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) can inhibit the development of colon cancer [1]; recent research evidence that epoxy The enzyme 2 (COX-2) is involved in many of the biological processes involved in tumorigenesis and development [2]. Unlike the previous concept of nucleotide metabolism as an anti-cancer core, COX-2 has become a new target for cancer prevention and treatment. A large number of epidemiological and clinical studies have confirmed that COX-2 and its catalyzed production of prostaglandin products are closely related to the evolution of tumors. Selective COX-2 inhibitors may hinder the development of malignant tumors [2].