Aspirin
產(chǎn)品名稱:Aspirin
產(chǎn)品描述:
| 產(chǎn)品描述 | 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. |
| 靶點活性 | COX-2:210 μg/mL, COX-1:5μg/mL |
| 體內(nèi)活性 | 當(dāng)中性粒細胞和人臍靜脈內(nèi)皮細胞共培養(yǎng)時,Aspirin可引起一種類花生酸的跨細胞生物合成,通過引起乙?;腜GHS-2和5-脂氧合酶相互作用形成。Aspirin可抑制NF-κB活化,防止其抑制劑,IκB的降解,使NF-κB保留在細胞質(zhì)中。在轉(zhuǎn)染的T細胞中,Aspirin也會抑制NF-κB依賴性Igκ增強子和HIV長末端重復(fù)序列的轉(zhuǎn)錄。在某種程度上, Aspirin和水楊酸鹽被其對IKK-β的特定抑制介導(dǎo),進而阻止涉及炎癥反應(yīng)發(fā)病機理的NF-κB基因激活。 Aspirin抑制IRS-1的Ser307磷酸化和JNK,c-Jun磷酸化,以及經(jīng)TNF-α處理的3T3-L1和Hep G2細胞中IkappaBalpha的降解。Aspirin抑制Akt磷酸化,并抑制rapamycin 的哺乳動物靶點對TNF-α的響應(yīng)。經(jīng)TNF-α預(yù)處理的3T3-L1脂肪細胞中,Aspirin可減少胰島素誘導(dǎo)的葡萄糖攝取。在大鼠神經(jīng)元原代培養(yǎng)物和海馬腦片中,Aspirin可降低由興奮性氨基酸谷氨酸引發(fā)的神經(jīng)毒性。 |
| 細胞實驗 | 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]. |
| 別名 | 阿司匹林, ASA, Acetylsalicylic Acid, 鄰乙酰水楊酸, Acetylsalicylate |
| 分子量 | 180.16 |
| 分子式 | C9H8O4 |
| CAS No. | 50-78-2 |
存儲
Powder: -20°C for 3 years | In solvent: -80°C for 2 years
溶解度
DMSO: 18 mg/mL (100 mM)
( < 1 mg/mL refers to the product slightly soluble or insoluble )
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