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Aspirin

CAS No. : 50⁻⁷8-2

MCE 国际站：Aspirin

产品活性：Aspirin是非选择性和不可逆的 COX-1 和 COX-2 抑制剂，IC₅₀ 分别为5，210 µg/mL。

研究领域：Immunology/Inflammation | Autophagy | Anti-infection

作用靶点：COX | Autophagy | Mitophagy | Virus Protease

In Vitro: Aspirin and other non-steroid anti-inflammatory drugs inhibit the activity of cyclooxygenase (COX) which leads to the formation of prostaglandins (PGs) that cause inflammation, swelling, pain and fever. Aspirin acetylates serine-530 of cyclooxygenase-1 (COX-1), thereby blocking thromboxane A synthesis in platelets and reducing platelet aggregation. This mechanism of action accounts for the effect of aspirin on prevention of coronary artery and cerebrovascular thrombosis. Aspirin is less effective in inhibiting COX-2 activity. Aspirin and salicylate inhibit COX-2 protein expression through interference with binding of CCAAT/enhancer binding protein beta (C/EBPbeta) to its cognate site on COX-2 promoter/enhancer. Aspirin inhibits the activation of NF-κB. This inhibition prevents the degradation of the NF-κB inhibitor, 1κB, and therefore NF-κB is retained in the cytosol. Aspirin also inhibits NF-κB-dependent transcription from the lgκ enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells. Aspirin inhibits COX-1 and COX-2 with IC₅₀ values of 3.57 µM and 29.3 µM, respectively in human articular chondrocytes.

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