|A unique collection of 81 Cardioprotective natural compounds for high throughput screening (HTS) and high content screening (HCS).|
|Catalog No:||Bb1313|| Cardioprotective Compound Library
|Size:||1mg/well * 81 Compounds|
2mg/well * 81 Compounds
1. Neferine shows significant improvement in cognitive impairment in scopolamine-induced amnesia animal models and moderate inhibitory activities, the anti-amnesic effect of neferine may be mediated via antioxidant and anti-inflammatory capacities, as well as inhibition of ChEs and BACE1.
2. Neferine induces autophagy through the inhibition of PI3K/Akt/mTOR pathway and ROS hyper generation in A549 cells.
3. Neferine attenuates bleomycin-induced pulmonary fibrosis in vitro and in vivo, the beneficial effect of neferine may be associated with its activities of anti-inflammation, antioxidation, cytokine and NF-kappaB inhibition.
4. Neferine has effects similar to rosiglitazone in decreasing fasting blood glucose, insulin, triglycerides (TG), tumor necrosis factor-alpha (TNF-alpha) and enhancing insulin sensitivity in insulin resistant rats.
5. Neferine inhibits proliferation of human osteosarcoma cells by promoting p38 MAPK-mediated p21 stabilization.
6. Neferine shows anti-anxiety effects and that neferine may participate in the efficacy of the sedative effects of embryos of the seeds of Nelumbo nucifera, the mechanisms of the sedative effects of neferine are not similar to those of diazepam.
7. Neferine possesses a significant inhibitory effect on amiodarone-induced pulmonary fibrosis, probably due to its properties of anti-inflammation, surfactant protein-D (SP-D) inhibition and restoring increased CD4+CD25+ Tregs which may modulate Th1/Th2 imbalance by suppressing Th2 response.
8. Neferine shows antidepressant-like effects in mice similar to typical antidepressants and that these effects are mediated by the 5-HT 1A receptor.
9. Neferine exerts strong antioxidant property against isoproterenol-induced oxidative stress and can be used as a potent cardioprotective agent against isoproterenol-induced myocardial infarction.
1. Methyl protodioscin shows strong cytotoxicity against most cell lines from solid tumors with GI50 ≤10.0 microM, but moderate cytotoxicity is shown against leukemia cell lines with GI50 10-30 microM.
2. Methyl protodioscin potentially increase HDL cholesterol while reducing LDL cholesterol and triglycerides.
3. Methyl protodioscin induced apoptotic process in human A549 cells is closely associated with Mitochondrial membrane potential, mitochondrial cytochrome c and caspase-3 .
4. Methylprotodioscin (50 mg/kg/d) can significantly inhibit bone loss in bone mineral content and bone mineral density in total, cancellous and cortical bones, and the decrease in bone strength indexes induced by ovariectomized , without side effect on the uterus; suggests that it has antiosteoporotic activity in vivo.
5. Methylprotodioscin and dioscin suppress the gene expression and production of MUC5AC mucin, by directly acting on airway epithelial cells, and the results are consistent with the traditional use of Asparagus cochinchinensis as remedy for diverse inflammatory pulmonary diseases.
6. Methyl protodioscin can inhibit the in-vitro thrombosis,decrease the dry and wet weight of thrombus and delay the occlusion time (OT), it has the effects of lowering the whole blood viscosity and plasma viscosity.
7. Methyl protodioscin has therapeutic effects on myocardial infarction in rats, it can reduce the level of myocardium enzyme and the myocardial infarction size,and increase the capability of clearing oxygen free radical and function of the vascular endothelial cell.
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. Ginkgolide C is a potent inhibitor of collagen-stimulated platelet aggregation, it may increase intracellular cAMP and cGMP production and MMP-9 activity, inhibit intracellular Ca(2+) mobilization and TXA(2) production, thereby leading to inhibition of platelet aggregation, it may be a suitable tool for a negative regulator during platelet activation.
2. Ginkgolide C has anti-adipogenic effect, it is an effective flavone for increasing lipolysis and inhibiting adipogenesis in adipocytes through the activated AMPK pathway.
3. Ginkgolide C can increase△LVP significantly,enhances the myocardial systolic and diastolic function of rats,but has no significant effect on HR while it shows inotropic activity.
1. Ginkgolide B (GB) has potent neuroprotective effects against ischemia-induced brain injury in vivo and in vitro, GB's neuroprotection is attributable to its anti-inflammatory and anti-apoptotic effect through inhibition of NF-κB.
2. Ginkgolide B may be therapeutically useful in the treatment of CNV and inflammation. 3. Ginkgolide B might be a promising drug on inhibiting platelet function and reducing inflammation in atherosclerosis.
4. Ginkgolide B alleviates endothelial dysfunction by reducing oxidative stress and elevating NO bioavailability and H2S production .
5. Ginkgolide B retards the proliferation and development of mouse embryonic stem cells (ESCs) and blastocysts in vitro and causes developmental injury in vivo.
6. Ginkgolide B can protect isolated hearts against arrhythmias induced by ischemia but not reperfusion.