Aspirin 是一种选择性 COX 抑制剂，具有多种药理活性。它是组蛋白去乙酰化酶抑制剂，可上调细胞周期阻滞蛋白 p21，抑制携带 COX-1 的卵巢 Y 细胞。 它还抑制 HUVEC 和新生大鼠心室心肌细胞中 COX-2 的表达，分别减少 PG 的产生和 ERK 和 NF-KB 的下调。

Acetylsalicylic acid is a potent and selective inhibitor of COX with various pharmacological activities, such as anti-inflammation and pain relief. Acetylsalicylic acid is a histone deacetylase inhibitors to up-regulate cell cycle arrest protein p21, which can suppresses ovarian Y cells harboring COX-1. Acetylsalicylic acid also inhibits the expression of COX-2 in HUVEC and neonatal rat ventricular cardiomyocytes, and then reduce PG production and the down-regulation of ERK and NF-KB, respectively.

当中性粒细胞和人脐静脉内皮细胞共培养时,Aspirin可引起一种类花生酸的跨细胞生物合成,通过引起乙酰化的PGHS-2和5-脂氧合酶相互作用形成。Aspirin可抑制NF-κB活化,防止其抑制剂,IκB的降解,使NF-κB保留在细胞质中。在转染的T细胞中,Aspirin也会抑制NF-κB依赖性Igκ增强子和HIV长末端重复序列的转录。在某种程度上, Aspirin和水杨酸盐被其对IKK-β的特定抑制介导,进而阻止涉及炎症反应发病机理的NF-κB基因激活。 Aspirin抑制IRS-1的Ser307磷酸化和JNK,c-Jun磷酸化,以及经TNF-α处理的3T3-L1和Hep G2细胞中IkappaBalpha的降解。Aspirin抑制Akt磷酸化,并抑制rapamycin 的哺乳动物靶点对TNF-α的响应。经TNF-α预处理的3T3-L1脂肪细胞中,Aspirin可减少胰岛素诱导的葡萄糖摄取。在大鼠神经元原代培养物和海马脑片中,Aspirin可降低由兴奋性氨基酸谷氨酸引发的神经毒性。

Chondrocytes are isolated from articular cartilage of donors with no articular disease. Unstimulated and interleukin 1 (IL-1) stimulated chondrocytes are used as models to study the effects of drugs on COX-1 and COX-2. Cells are incubated with vehicle or drugs (Asprin); supernatants are removed and the level of prostaglandin E2 (PGE2) in each sample is determined by enzyme immunoassay. IC50s are calculated from the reduction in PGE2 content by different concentrations of the test substance by linear regression analysis[5].

50-78-2

C9H8O4

180.159

邻乙酰水杨酸;阿司匹林;ASA;Acetylsalicylic Acid;Acetylsalicylate

DMSO:18 mg/mL (100 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years