|A unique collection of 51 Anti-platelet aggregation natural compounds|
|Catalog No:||B24|| Anti-platelet-aggregation Compound Library
|Size:||1mg/well * 51 Compounds|
2mg/well * 51 Compounds
1. Rubiarbonol B may have antiplatelet aggregation activities.
Chrysophanol-8-O-beta-D-glucopyranoside and chrysophanol have mild cytotoxicity and anti-diabetic properties and can play metabolic roles in the insulin-stimulated glucose transport pathway; it has potent inhibitory effect on collagen- and thrombin-induced platelet aggregation, it only inhibits platelet phosphatidylserine exposure.Chrysophanol-8-O-beta-D-glucopyranoside also exhibits significant anti-HBV activities with improved liver function, and enhanced HBeAg and HBsAg sero-conversion rates as well as HBV DNA clearance rates in HepG2 2.2.15 cells, DHBV models, or patients with chronic hepatitis B (CHB).
Pomolic acid has anti-cancer, anti-inflammatory and apoptotic activities, it can induce apoptosis in SK-OV-3 cells, which is mediated by the mitochondrial-mediated intrinsic and death receptor-induced extrinsic pathways. Pomolic acid is a potent inhibitor of the aggregation of human platelets induced by ADP and Epinephrine, exhibits IC50 values close to 60 nM and 20 nM, respectively; pomolic acid does not inhibit human platelet aggregation induced by PAF, collagen, U46619 (thromboxane analogue), TRAP or arachidonic acid; suggests that the hypotensive and platelet anti-aggregating effects of pomolic acid and its potential role in cardiovascular therapy.
Ginkgolide J has neuroprotective activity, it can prevent A beta(1-42) induced inhibition of long-term potentiation in the CA1 region of mouse hippocampal slices, it is also capable of inhibiting cell death of rodent hippocampal neurons caused by A beta(1-42). Ginkgolide J can inhibit platelet aggregation induced by ADP or PAF.
|CFN99161||Salvianolic acid A
Salvianolic acid A has antioxidant, hepatoprotective, antithrombotic effect, and antiplatelet actions. it also has a significant protective effect against isoproterenol-induced myocardial infarction; it activates the Nrf2/HO-1 axis in RPE cells and protects against oxidative stress via activation of Akt/mTORC1 signaling. Salvianolic acid A (oral) can significantly improve glucose metabolism and inhibit oxidative injury as well as protect against impaired vascular responsiveness in STZ-induced diabetic rats. It is a novel matrix metalloproteinase-9 inhibitor, can prevents cardiac remodeling in spontaneously hypertensive rats.