Product name: Loureirin A
Synonym name:
Catalogue No.: BP3235
Cas No.: 119425-89-7
Formula: C₁₇H₁₈O₄
Mol Weight: 286.327
Botanical Source:
Physical Description: Powder
Type of Compound: Chalcones

Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle
The product could be supplied from milligrams to grams. Inquire for bulk scale.
We provide solution to improve the water-solubility of compounds, thereby facilitating the variety of activity tests and clinic uses.

For Reference Standard and R&D, Not for Human Use Directly.

Description:

Loureirin A has an inhibitory effect on platelet activation, perhaps through an impairment of PI3K/Akt signaling. Loureirin A activates Wnt/-catenin pathway and promotes hair follicle stem cells (FSCs)-seeded tissue-engineered skin to repair skin wound.The molecular mechanism of Loureirin A and Wnt signaling pathway mediated anti- hepatic fibrosis and anti- angiogenesis may involve down- regulation the expression of Frizzled- 4,inhibiting the synthesis and secretion of α- SMA,TGF- β1and the proliferation of HSCs.

References:

Eur J Pharmacol. 2015 Jan 5;746:63-9.    

Antiplatelet activity of loureirin A by attenuating Akt phosphorylation: In vitro studies.   

Loureirin A is a flavonoid extracted from Dragon׳s Blood that has been used to promote blood circulation and remove stasis in Chinese traditional medicine. However, the mechanisms of these effects are not fully understood. 

METHODS AND RESULTS:

We explored the anti-platelet activity and underlying mechanism of Loureirin A in vitro. Our results indicated that Loureirin A negatively affected agonist-induced platelet aggregation such as collagen, collagen-related peptide (CRP), ADP and thrombin. Loureirin A inhibited collagen-induced platelet ATP secretion and thrombin-stimulated P-selectin expression in a dose-dependent manner. Platelet spreading on immobilized fibrinogen was significantly impaired in the presence of Loureirin A. Immunoblotting analysis indicated that 100μM of Loureirin A almost completely eliminated collagen-induced Akt phosphorylation at Ser473. Interestingly, a submaximal dose (50μM) of Loureirin A had an additive inhibitory effect with the phosphoinositide 3-kinase (PI3K) inhibitor Ly294002 on collage-induced Akt phosphorylation in platelets. 

CONCLUSIONS:

Taken together, Loureirin A had an inhibitory effect on platelet activation, perhaps through an impairment of PI3K/Akt signaling.    

Journal of Kunming Medical University, 2016 , 37 (6) :13-17.    

Effect of Loureirin A on Proliferation and Frizzled-4Expression of Rat Hepatic Stellate Cells in vitro    

To investigate the molecular mechanism of Loureirin A mediated anti- hepatic fibrosis by evaluting its effects on proliferation,secretion of α- smooth muscle actin(α- SMA) and transforming growth factor- beta1(TGF- β1), and expression of rat hepatic stellate cells in vitro. 

METHODS AND RESULTS:

Primary hepatic stellate cells were isolated and cultured from Sprague- Dawley rats. After activating and inducing primary hepatic stellate cells from q HSC to a HSC, the activated hepatic stellate cells model in vitro was established. Then we observed the morphological changes of static hepatic stellate cells and activated hepatic stellate cells with inverted phase contrast microscope. Cultured hepatic stellate cells were treated with different concentrations of Loureirin A and the inhibitory rate of HSCs proliferation was measured by MTT assay. The expression of Frizzled- 4 was measured by western blot analysis. The content of α- SMA and TGF- β1 in the cultured HSCs' supernatant were measured by enzyme- linked immunosorbent assay(ELISA). Loureirin A the proliferation of inhibited activated hepatic stellate cells in a time- dose- dependent manner compared with the control group,IC50=0.30 μg/μL. After Loureirin A treatment of the HSCs, western blot analysis showed that Frizzled- 4 expression level was obviously lower than control group.Loureirin A also inhibited α- SMA and TGFβ1(P0.05) secretion in the cultured HSCs' supernatant in different degree by the assay of ELISA. 

CONCLUSIONS:

The molecular mechanism of Loureirin A and Wnt signaling pathway mediated anti- hepatic fibrosis and anti- angiogenesis may involve down- regulation the expression of Frizzled- 4,inhibiting the synthesis and secretion of α- SMA,TGF- β1and the proliferation of HSCs.