CAS NO: | 18642-23-4 |
包装 | 价格(元) |
5mg | 电议 |
10mg | 电议 |
25mg | 电议 |
100mg | 电议 |
Cas No. | 18642-23-4 |
别名 | 补骨脂定 |
化学名 | 3,9-dihydroxy-2-(3-methyl-2-buten-1-yl)-6H-benzofuro[3,2-c][1]benzopyran-6-one |
Canonical SMILES | OC1=CC(O2)=C(C=C1)C3=C2C4=C(OC3=O)C=C(O)C(C/C=C(C)/C)=C4 |
分子式 | C20H16O5 |
分子量 | 336.3 |
溶解度 | ≤14mg/ml in DMSO;14mg/ml in dimethyl formamide |
储存条件 | Store at -20℃ |
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
Shipping Condition | Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request |
产品描述 | Psoralidin is a dual inhibitor of COX-2 and 5-LOX. Psoralidin, a coumestan derivative isolated from seed of Psoralea corylifolia, has been widely used in traditional medicine for bleeding, pollakiuria, enuresis, vitiligo, and psoriasis. Psoralidin shows a variety of biological activities such as anti-cancer, anti-bacterial, anti-oxidant, anti-depressant activities and regulation of insulin signaling [1]. Psoralidin (100 μM) inhibited COX-2 in IR-irradiated normal lung fibroblasts in HFL-1 and MRC-5 cells [1]. Psoralidin significantly inhibited IR-induced NF-κB-luciferase activity. Psoralidin inhibited the IR-induced COX-2 expression and PGE2 production through regulation of PI3K/Akt and NF-κB pathway. Also, psoralidin blocked IR-induced LTB4 production through direct interaction with 5-lipoxygenase activating protein (FLAP) in 5-LOX pathway. Psoralidin significantly attenuated IR-induced fibroblast migration [1]. Psoralidin inhibited LPS-induced iNOS expression via repressing Syk-mediated activation of PI3K-IKK-IκB signaling pathways [2]. Psoralidin enhanced TRAIL-induced apoptosis in HeLa cells through increased expression of TRAIL-R2 death receptor and depolarization of mitochondrial membrane potential [3]. In male BALB/c strain mice (eight weeks, average weight 22–25 g), psoralidin (5 mg/kg) suppressed IR-induced expression of pro-inflammatory cytokines (TNF-α, TGF-β, IL-6 and IL-1 α/β) and ICAM-1 [1]. References: |