product name Aspirin
Description: Aspirin (also known as Acetylsalicylic acid) is a salicylate, and irreversible COX1 and COX2 inhibitor. Aspirin has a broad range of pharmacological activities including anti-inflammation and pain relief and is used as an analgesic to relieve minor aches and pains, as an antipyretic to reduce fever, and as an anti-inflammatory medication. Aspirin suppresses ovarian cancer cells harboring COX-1 by acting as histone deacetylase inhibitors to up-regulate cell cycle arrest protein p21.
References: Science. 1994 Aug 12;265(5174):956-9; Nature. 1998 Nov 5;396(6706):77-80.
180.16
Formula
C9H8O4
CAS No.
50-78-2
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 36 mg/mL (199.8 mM)
Water: <1 mg/mL
Ethanol: 36 mg/mL (199.8 mM)
Solubility (In vivo)
4% DMSO+PBS: 10mg/mL
Synonyms
Acetylsalicylic acid
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19408049
| In Vitro |
In vitro activity: Aspirin inhibits the activation of NF-kappa B, thus prevents the degradation of the NF-kappa B inhibitor, I kappa B, and therefore NF-kappa B is retained in the cytosol. Aspirin also inhibits NF-kappa B-dependent transcription from the Ig kappa enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells. Aspirin and salicylate are mediated in part by their specific inhibition of IKK-beta, thereby preventing activation by NF-kappaB of genes involved in the pathogenesis of the inflammatory response. Aspirin is protective against neurotoxicity elicited by the excitatory amino acid glutamate in rat primary neuronal cultures and hippocampal slices. Aspirin triggers transcellular biosynthesis of a previously unrecognized class of eicosanoidsduring coincubations of human umbilical vein endothelial cells (HUVEC) and neutrophils [polymorphonuclear leukocytes (PMN)]. Aspirin evokes a unique class of eicosanoids formed by acetylated PGHS-2 and 5-lipoxygenase interactions. Aspirin treatment inhibits the phosphorylation of IRS-1 at Ser307 as well as the phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha in 3T3-L1 and Hep G2 cells treated with tumor necrosis factor (TNF)-alpha. Aspirin treatment inhibits phosphorylation of Akt and the mammalian target of rapamycin (but not extracellular regulated kinase or PKCzeta) in response to TNF-alpha. Aspirin rescues insulin-induced glucose uptake in 3T3-L1 adipocytes pretreated with TNF-alpha. Kinase Assay: Cell Assay: |
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| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | Science. 1994 Aug 12;265(5174):956-9; Nature. 1998 Nov 5;396(6706):77-80. |
