Loureirin A

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

Loureirin A 对血小板活化具有抑制作用，可能是通过损害 PI3K/Akt 信号传导来实现的。Loureirin A 对激动剂诱导的血小板聚集（如胶原蛋白、胶原相关肽 (CRP)、ADP 和凝血酶）产生负面影响。

Loureirin A has an inhibitory effect on platelet activation perhaps through an impairment of PI3K/Akt signaling.Loureirin A negatively affects agonist-induced platelet aggregation such as collagen collagen-related peptide (CRP) ADP and thrombin. 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- 4inhibiting the synthesis and secretion of α- SMATGF- β1and the proliferation of HSCs.

Loureirin A (50 μM, 100 μM) inhibits collagen-induced platelet ATP secretion and thrombin-stimulated P-selectin expression in a dose-dependent manner. Loureirin A also significantly impairs platelet spreading on immobilized fibrinogen. Loureirin A almost completely eliminates collagen-induced Akt phosphorylation at Ser473 at the dose of 100 μM, and has an additive inhibitory effect with the phosphoinositide 3-kinase (PI3K) inhibitor Ly294002 on collage-induced Akt phosphorylation in platelets at 50 μM.

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PI3K/Akt/mTOR signaling

PI3K

PI3K

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119425-89-7

286.32

C17H18O4

>98% (HPLC)

DMSO: ≥ 86.6 mg/mL (302.46 mM)

COc1ccc(CCC(=O)c2ccc(O)cc2)c(OC)c1

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(-20℃)

With Ice Pack

≥ 2 years