1. Liquiritin can increase SOD activity, inhibit lipid peroxidation, and lessen production of MDA, demonstrates that a potential antidepressant-like effect of liquiritin treatment on chronic variable stress can induce depression model rats, which might be related to defense of liquiritin against oxidative stress.
2. Liquiritin has neuroprotective effect against focal cerebral ischemia/reperfusion in mice via its antioxidant and antiapoptosis properties, it may be a potential agent against cerebral I/R injury in mice.
3. Liquiritin significantly promotes the neurite outgrowth stimulated by NGF in PC12 cells in dose dependant manners , it may be a good candidate for treatment of various neurodegenerative diseases such as Alzheimer’s disease or Parkinson’s disease.
4. Liquiritin can attenuate advanced glycation end products-induced endothelial dysfunction via RAGE/NF-κB pathway in human umbilical vein endothelial cells, it may be a promising agent for the treatment of vasculopathy in diabetic patients.
|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.
1. Ginkgolide A has neuroprotective effects.
2. Ginkgolide A is widely used for the treatment of cardiovascular diseases and diabetic vascular complications, which might be achieved through regulating the STAT3-mediated pathway.
3. Ginkgolide A could increase cell viability and suppress the phosphorylation level of Tau in cell lysates, meanwhile, GSK3β was inhibited with phosphorylation at Ser9.
4. Ginkgolide A promoted phosphorylation of PI3K and Akt, suggesting that the activation of the PI3K-Akt signaling pathway may be the mechanism to prevent the intracellular accumulation of p-Tau induced by okadaic acid and to protect the cells from Tau hyperphosphorylation-related toxicity.
5. Ginkgolide A has anxiolytic-like effect in mice.
6. Ginkgolide A is a platelet-activating factor antagonist, it can inhibit the neurotoxicity of prions or amyloid-beta1-42, may be relevant treatments for prion or Alzheimer's diseases.
1. Cyanidin-3- O -glucoside has protective effects from blackberry extract against peroxynitrite-induced endothelial dysfunction and vascular failure.
2. Cyanidin-3- O -glucoside exhibits strong antioxidant activities including DPPH radical scavenging activities, ABTS radical scavenging activities and ORAC values.
3. Cyanidin-3-O-glucoside chloride decreases mutant p21 expression, and increases the ratio of Bax/Bcl-2 and the activation of caspase-3 to induce apoptosis.
1. Bilirubin is a potent antioxidant.
2. Bilirubin may compromise cellular metabolism and proliferation via induction of ER stress.