Hydroxysafflor yellow A - CAS 78281-02-4
Catalog number: B0084-474840
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C27H32O16
Molecular Weight:
612.53
COA:
Inquire
Targets:
Others
Description:
Hydroxysafflor yellow A is a flavonoid derived. It is extracted from traditional Chinese medicine Carthamus tinctorius L. It possesses anti-tumor activity. It could inhibit LPS-induced VSMCs proliferation and migration, and inhibited LPS-induced upregulation of TLR-4 expression in vitro. It attenuated LPS triggered ICAM-1 and E-selectin mRNA levels elevation and phosphorylation of p38 MAPK or c-Jun N-terminal kinase MAPK. It inhibited the proliferation of 3T3-L1 preadipocytes and cell viability greatly decreased in a dose and time dependent manner. It inhibited adipogenesis by increasing HSL promoter activities. It can effectively protect the liver from long-term alcohol injury by enhancing antioxidant capacity and inhibiting the expression of TGF-β. It prevents steroid-induced avascular necrosis of femoral head by inhibiting primary bone marrow-derived mesenchymal stromal cells.
Ordering Information
Catalog Number Size Price Stock Quantity
B0084-474840 100 mg $198 In stock
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Purity:
>98%
Appearance:
Solid powder
Synonyms:
(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;2,5-Cyclohexadien-1-one, 2,4-di-beta-D-glucopyranosyl-3,4,5-trihydroxy-6-((2E)-3-(4-hydroxyphenyl)-1-oxo-2-propenyl)-;SaffloMin A;HSYA
Solubility:
DMSO: 39 mg/mL
Storage:
-20°C Freezer
MSDS:
Inquire
Application:
Hydroxysafflor yellow A could inhibit LPS-induced VSMCs proliferation and migration, and inhibited LPS-induced upregulation of TLR-4 expression in vitro. It attenuated LPS triggered ICAM-1 and E-selectin mRNA levels elevation and phosphorylation of p38 MAPK or c-Jun N-terminal kinase MAPK. It inhibited adipogenesis by increasing HSL promoter activities. It can effectively protect the liver from long-term alcohol injury by enhancing antioxidant capacity and inhibiting the expression of TGF-β. It prevents steroid-induced avascular necrosis of femoral head by inhibiting primary bone marrow-derived mesenchymal stromal cells.
Quality Standard:
In-house standard
Shelf Life:
2 month in rt, long time
Quantity:
Grams to Kilograms
Boiling Point:
1015.8±65.0 °C | Condition: Press: 760 Torr
Melting Point:
184-186 °C
Density:
1.851±0.06 g/cm3 | Condition: Temp: 20 °C Press: 760 Torr
InChIKey:
IAVUBSCVWHLRGE-UXEKTNMQSA-N
InChI:
InChI=1S/C27H32O16/c28-7-12-16(32)19(35)21(37)23(42-12)15-18(34)14(11(31)6-3-9-1-4-10(30)5-2-9)24(39)27(41,25(15)40)26-22(38)20(36)17(33)13(8-29)43-26/h1-6,12-13,16-17,19-23,26,28-38,41H,7-8H2/b6-3+,14-11+/t12-,13-,16-,17-,19+,20+,21-,22-,23+,26-,27?/m1/s
Canonical SMILES:
C1=CC(=CC=C1C=CC(=C2C(=C(C(=O)C(C2=O)(C3C(C(C(C(O3)CO)O)O)O)O)C4C(C(C(C(O4)CO)O)O)O)O)O)O
1.Hydroxysafflor yellow A increases BDNF and NMDARs in the hippocampus in A vascular dementia rat model.
Mengya X1, Qingna S1, Yiyi W2, Yan C1, Nan Z3. Brain Res. 2016 Apr 14. pii: S0006-8993(16)30253-0. doi: 10.1016/j.brainres.2016.04.030. [Epub ahead of print]
Hydroxysafflor yellow A (HSYA) is a drug that exerts angiogenesis regulatory and neuroprotective effects and has become an effective therapy for brain and heart ischemic disorders. There is no definite evidence supporting a therapeutic effect of HSYA in vascular dementia (VaD). We used HSYA in a rat model of chronic cerebral ischemia to determine its potential therapeutic effects in VaD. The Morris water maze (MWM) was used to evaluate spatial cognitive function, and long-term potentiation (LTP) was tested as a marker of synaptic plasticity. The expression levels of brain-derived neurotrophic factor (BDNF) and two subunits of N-methyl-d-aspartate receptor (NMDAR; GluN2A and GluN2B) in the hippocampus were measured via western blotting. The MWM results showed that the experimental VaD group had longer escape latencies than the sham group, whereas the HSYA group had a decreased escape latency compared with the VaD group (P<0.05). The LTP at CA3-CA1 synapses in the hippocampus was also enhanced in the HSYA compared with the VaD group (P<0.
2.Antioxidant effects of hydroxysafflor yellow A and acetyl-11-keto-β-boswellic acid in combination on isoproterenol-induced myocardial injury in rats.
Chen M1, Wang M1, Yang Q1, Wang M2, Wang Z2, Zhu Y1, Zhang Y1, Wang C1, Jia Y1, Li Y1, Wen A1. Int J Mol Med. 2016 Apr 20. doi: 10.3892/ijmm.2016.2571. [Epub ahead of print]
Oxidative stress plays an important role in the initiation and development of myocardial injury (MI). The peroxisome proliferator-activated receptor gamma coactivator-1α (PGC‑1α)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway is considered to be a potential target for cardioprotection in MI. Acetyl-11-keto-β-boswellic acid (AKBA) is the major organic acid component extracted from Boswellia serrata Roxb. ex Colebr. Hydroxysafflor yellow A (HSYA) is the principal active constituent of Carthamus tinctorius L. In the present study, we aimed to investigate the cardioprotective effects of HSYA and AKBA in combination in vivo and in vitro, as well as the underlying mechanisms responsible for these effects. For this purpose, MI was produced in Sprague-Dawley rats by subcutaneous injection with isoproterenol. To model ischemic-like conditions in vitro, H9C2 cells were subjected to oxygen-glucose deprivation (OGD). The levels of creatine kinase-MB (CK‑MB), lactate dehydrogenase (LDH), malondialdehyde (MDA) as well as superoxide dismutase (SOD) activity were examined as well as apoptotic cell death.
3.Hydroxysafflor Yellow A Ameliorates Renal Fibrosis by Suppressing TGF-β1-Induced Epithelial-to-Mesenchymal Transition.
Hu N1,2, Duan J1,2, Li H1,2, Wang Y2, Wang F1,2, Chu J1,2, Sun J1,2, Liu M1, Wang C1, Lu C1, Wen A1,2. PLoS One. 2016 Apr 18;11(4):e0153409. doi: 10.1371/journal.pone.0153409. eCollection 2016.
OBJECTIVE: Renal fibrosis is the common pathological foundation of many chronic kidney diseases (CKDs). The aim of this study was to investigate whether Hydroxysafflor yellow A (HSYA) can preserve renal function by inhibiting the progression of renal fibrosis and the potential mechanisms.
4.Hydroxysafflor yellow A improves established monocrotaline-induced pulmonary arterial hypertension in rats.
Han X1, Zhang Y2, Zhou Z1, Zhang X1, Long Y1. J Int Med Res. 2016 Apr 8. pii: 0300060515597931. [Epub ahead of print]
OBJECTIVE: To evaluate the beneficial effects of hydroxysafflor yellow A (HSYA) on monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) in rats, and to investigate the main pathophysiological mechanism of HSYA in preventing development of MCT-induced PAH.
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CAS 78281-02-4 Hydroxysafflor yellow A

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