摘要
NSAIDs的抗炎作用机制被认为主要是抑制COX2的活性。NSAIDs还可以抑制COX2的表达,并可通过COX非依赖性的途径产生抗炎作用,包括抑制转录因子NFκB与AP1,作用于蛋白激酶如Erk、p38MAPK、及核糖体S6激酶2等,激活PPARγ及热休克转录因子1,抑制诱导型NO合酶及前列腺素转运等。
The anti-inflammatory mechanism of nonsteroidal anti-inflammatory drugs （NSAIDs） is mainly due to inhibition of COX-2 activity. NSAIDs can also inhibit COX-2 expression and produce anti-inflammatoinhibit COX-2 expression and produce anti-inflammatory effect independent of COX. These COX-independent mechanisms include inhibiting transcription factors such as NF-κB and AP-1, interfering with signal trans-duction pathways through actions on Erk,p38MAPK,IKK and RSK2, activating PPARγ
and HSF-1, inhibiting iNOS and transport of prostanoids from their generating cells.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2005年第8期905-910,共6页
Chinese Pharmacological Bulletin
基金
中国高技术研究发展计划(863计划)重大专项基金资助课题(No2004AA2Z3782)
