產(chǎn)品屬性：
產(chǎn)品名稱 | Hydroxysafflor yellow A |
規(guī)格 | 20mg |
貨號(hào) | EY-01Y19581 |
Cas No.: 78281-02-4
別名: Safflomin A
化學(xué)名: (6E)-2,5-dihydroxy-6-[(E)-1-hydroxy-3-(4-hydroxyphenyl)prop-2-enylidene]-2,4-bis[(2S,3R,4R,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]cyclohex-4-ene-1,3-dione
分子式: C27H32O16
分子量: 612.53
溶解度: ≥ 61mg/mL in H2O, ≥ 61.3mg/mL in DMSO
儲(chǔ)存條件: 4°C, protect from light
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
產(chǎn)品描述：
Hydroxysafflor yellow A is a flavonoid derived and isolated from traditional Chinese medicine Carthamus tinctorius L., possesses anti-tumor activity. IC50 value:Target: in vitro: HYSA could inhibit LPS-induced VSMCs proliferation and migration, accompanied by the downregulated levels of several key pro-inflammatory cytokines, including TNF-α, IL-6, and IL-8. We further showed that HYSA inhibited LPS-induced upregulation of TLR-4 expression as well as the activation of Rac1/Akt pathway [1]. HSYA protected EC viability against LPS-induced injury (P<0.05). LPS-induced NF-κB p65 subunit DNA binding (P<0.01) and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor -α (I-κB-α) phosphorylation was inhibited by HSYA. HSYA attenuated LPS triggered ICAM-1 and E-selectin mRNA levels elevation and phosphorylation of p38 MAPK or c-Jun N-terminal kinase MAPK [2]. HSYA inhibited the proliferation of 3T3-L1 preadipocytes and cell viability greatly decreased in a dose and time dependent manner. HSYA (1 mg/l) notably reduced the amount of intracellular lipid and triglyceride content in adipocytes by 21.3 % (2.13 ± 0.36 vs 2.71 ± 0.40, P < 0.01) and 22.6 % (1.33 ± 0.07 vs 1.72 ± 0.07, P < 0.01) on days 8 following the differentiation, respectively [3]. in vivo: HSYA treatment ameliorated serum biochemical indicators by reducing the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronan (HA), laminin (LN), and type III precollagen (III-C) in rats [4].
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