|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.
1. Chrysophanol-8-O-glucoside has potent inhibitory effect on collagen- and thrombin-induced platelet aggregation, it only inhibits platelet phosphatidylserine exposure, but not exerts direct inhibition on intrinsic factors, suggests that it may be of therapeutic benefit for the prevention of platelet-related cardiovascular diseases.
2. 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.
3. Chrysophanol 8-O-beta-d-glucoside 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).
1. Pomolic acid, isolated from R. woodsii and H. capitata, was identified as an anti-HIV agent (EC50 1.4 microg/mL, T. I. 16.6).
2. Pomolic acid has anti-inflammatory and apoptotic activities.
3. Pomolic acid exerts anti-cancer properties through the modulation of AMP-activated protein kinase (AMPK) pathways and its value as an anti-cancer agent in breast cancer therapy.
4. 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.
5. Pomolic acid can induce apoptosis in SK-OV-3 cells, which is mediated by the mitochondrial-mediated intrinsic and death receptor-induced extrinsic pathways.
1. Ginkgolide J 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).
2. Ginkgolide J can inhibit platelet aggregation induced by ADP or PAF.
3. Ginkgolides (Gins A, B, C and J) have a significant role to protect the primary cortical neurons from hypoxic injury induced by potassium cyanide (KCN).
|CFN99161||Salvianolic acid A
1. Salvianolic acid A has protection against cerebral lesion, defense from oxidative damage and improvement of remembrance; it also has antithrombotic effect, antiplatelet action and can modulate hemorheology without affecting coagulation system, the mechanisms underlying such activities may involve the induction of cAMP.
2. Salvianolic acid A possesses antioxidant activity, 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.
3. 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.
4. Salvianolic acid A has protection on oxidative stress and liver injury induced by carbon tetrachloride in rats, which may mainly be related to its antioxidative effect.
5. Salvianolic acid A inhibits platelet activation via the inhibition of PI3K, and attenuates arterial thrombus formation in vivo, suggests that it may be developed as a novel therapeutic agent for the prevention of thrombotic disorders.
6. Salvianolic acid A is a novel matrix metalloproteinase-9 inhibitor, can prevents cardiac remodeling in spontaneously hypertensive rats.
7. Salvianolic acid A inhibits PDGF-BB-activated HSC proliferation, partially through apoptosis induction, it exerts no direct cytotoxicity on primary hepatocytes and HSC-T6 cells under experimental concentrations.