诱导型环氧合酶(COX-2)在炎症中的作用。

Receptor Pub Date : 1994-01-01
K Seibert, J L Masferrer
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引用次数: 0

摘要

非甾体抗炎药(NSAIDs)是一种有效的抗炎药,通过抑制环氧化酶(COX)酶和随后抑制炎症部位的前列腺素来起作用。不幸的是,胃肠道或肾脏前列腺素的抑制与基于机制的毒性有关,这限制了这些有效药物的有效性。最近已经确定了COX酶的两种形式:COX-1,在许多细胞和组织中组成性表达,COX-2,在炎症部位被促炎细胞因子选择性诱导。第二种COX酶的发现导致了一种假设,即与临床有用的非甾体抗炎药相关的毒性是由抑制COX-1引起的,而抗炎特性是由抑制诱导型COX-2引起的。为了支持这一假说,诱导型COX-2酶的表达被强效抗炎药物地塞米松选择性阻断。选择性抑制COX-2可能产生比现有非甾体抗炎药更安全的抗炎药。
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Role of inducible cyclooxygenase (COX-2) in inflammation.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are potent anti-inflammatory agents that act through the inhibition of the cyclooxygenase (COX) enzyme and the subsequent inhibition of prostaglandins at the site of inflammation. Unfortunately, inhibition of gastrointestinal or renal prostaglandins is associated with mechanism-based toxicities that limit the usefulness of these otherwise potent and efficacious drugs. Recently two forms of the COX enzyme have been identified: COX-1, which is constitutively expressed in many cells and tissues, and COX-2, which is selectively induced by proinflammatory cytokines at the site of inflammation. The discovery of a second COX enzyme led to the hypothesis that toxicity associated with the clinically useful NSAIDs is caused by the inhibition of COX-1, whereas the anti-inflammatory properties were caused by the inhibition of inducible COX-2. In support of this hypothesis, expression of the inducible COX-2 enzyme is selectively blocked by the potent anti-inflammatory drug dexamethasone. Selective inhibition of COX-2 may produce superior anti-inflammatory drugs with substantial safety over existing NSAIDs.

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