|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. Ursolic acid has anti-tumor, anti-inflammatory, antidepressant-like, antimicrobial activities, and anti-asthmatic effects.
2. Ursolic acid may have a potential application as a chemopreventive agent to prevent the metastasis of gastric cancer or to alleviate the process of metastasis.
3. Ursolic acid may ameliorate colitis by regulating NF-κB and MAPK signaling pathways via the inhibition of LPS binding to TLR4 on immune cells.
4. Ursolic acid has hepatoprotective action, can inhibit CCl4-induced liver fibrosis, inflammation and apoptosis, via at least in part to its ability to modulate the Nrf2/ARE signalling pathway.
5. Ursolic acid inhibits Hut-78 cells' proliferation and induced apoptosis through h death receptors and mitochondrial pathways, NF-κB classical signal pathway may be one of its mechanisms, and VEGF and cox-2 may also be involved.
6. Ursolic acid is a potential PPARγagonist, can suppress ovalbumin-induced airway inflammation and Penh by down-regulating IL-5, IL-13, and IL-17 in a mouse model of allergic asthma.
7. Ursolic acid has an antioxidant activity, it can ameliorate cognition deficits and attenuates oxidative damage in the brain of senescent mice induced by D-galactose, it may offer a novel therapeutic strategy for the treatment of age-related conditions.
8. Ursolic acid has antihyperlipidemic, hypoglycemic and direct cardiac effect, its antihypertensive effect is attributed to its potent diuretic-natriuretic-saluretic activity.
1. Visnagin and khellin can prevent renal epithelial cell damage caused by oxalate (Ox) and calcium oxalate monohydrate (COM) and can therefore play a potential role in the prevention of stone formation associated with hyperoxaluria.
2. Visnagin can relax aortae previously contracted by noradrenaline, and weakly inhibit the hydrolytic activity of the cyclic nucleotide phosphodiesterase (PDE) isozymes (PDE5, PDE4, PDE3, cyclic GMP activated PDE2 and PDE1).
3. Visnagin has acute hypotensive effect , the main mechanism is the vasorelaxant response induced by this drug in resistance arteries.
4. Visnagin has anti-inflammatory effect in lipopolysaccharide-stimulated BV-2 microglial cells, the main mechanism may result from the inhibition of transcription factors, such as AP-1 and NF-κB.
5. Visnagin protects against doxorubicin-induced cardiomyopathy through modulation of mitochondrial malate dehydrogenase.
6. Visnagin has neuroprotective effects on kainic acid-induced neuronal cell death in the mice hippocampus, the neuroprotective effects are associated with its anti-inflammatory effects.
1. Rutaecarpine has the potential for use as an anti-atherosclerosis agent with a novel mechanism.
2. Rutaecarpine promotes glucose consumption and improves insulin resistance possibly through suppression of inflammatory cytokines in the IR-PSMC cells.
3. Rutaecarpine is effective against Ang II-induced rat VSMC proliferation, at least in part, to NO production and the modulation of VMSC proliferation-related gene expressions.
4. Rutaecarpine is a potent inhibitor of CYP1A2 in both mouse and human liver microsome.
5. Rutaecarpine shows in vivo anti-inflammatory activity on rat lambda-carrageenan induced paw edema, which could be attributed at least in part by inhibition of COX-2.
6. Rutaecarpine has positive inotropic and chronotropic effects on the guinea-pig isolated right atria, possible involvement of vanilloid receptors.
7. Rutaecarpine exerts both antihypertensive and anti-platelet effects through stimulating the synthesis and release of CGRP in spontaneously hypertensive rats (SHR).
8. Rutaecarpine has vasorelaxing action, it has direct paradoxical effects on intracellular calcium concentration of vascular smooth muscle and endothelial cells.
9. Rutaecarpine has gastroprotective effects, it protects the gastric mucosa against injury induced by acetylsalicylic acid (ASA)and stress.
10. Rutaecarpine may be useful in the prevention of ultraviolet A-induced photoaging, it inhibits ultraviolet A-induced reactive oxygen species generation, resulting in the enhanced expression of matrix metalloproteinase (MMP)-2 and MMP-9 in human skin cells.
11. Rutaecarpine may cause immunosuppressive effects, which may be mediated, at least in part, through the inhibition of cytokine production and cell cycle arrest in G0 + G1 phase, and causes possibly by mechanisms associated with metabolic activation.
1. Nardosinone has inhibitory effect on Ang II-induced hypertrophy in H9c2 cells, might be mediated by targeting PI3K/Akt and MEK/ERK signaling pathways.
2. Nardosinone could protect against the neuronal injury exposed to OGD, which may be relevant to the promotion of PKA and ERK signaling pathway.
3. Nardosinone enhances staurosporine- or dbcAMP-induced neurite outgrowth from PC12D cells, probably by amplifying both the MAP kinase-dependent and -independent signaling pathways of dbcAMP and staurosporine.
4. The enhancement of NGF-induced neurite outgrowth from PC12D cells by Nardosinone involves activation of a down-stream step of the MAP kinase-dependent cascade of NGF coupled with PKC.
1. Glaucocalyxin A-SBE-β-CD could be useful with a better solubility and sustained function in drug delivery.
2. Glaucocalyxin A activates caspase-3, decreases BAD phosphorylation, and reduces the expression of X-linked inhibitor of apoptosis protein.
3. Glaucocalyxin A inhibits Akt phosphorylation, suppresses proliferation, and promotes apoptosis in a dose-dependent manner, but not in normal glial cells.
4. Glaucocalyxin A inhibits collagen-stimulated tyrosine phosphorylation of Syk, LAT, and phospholipase Cγ2, the signaling events in collagen receptor GPⅥ pathway.
5. Glaucocalyxin A could potentially be developed as an antiplatelet and antithrombotic agent, can inhibit platelet p-selectin secretion and integrin activation by convulxin, is a GPVI selective ligand.
6. Glaucocalyxin A has regulation of microglia activity, can attenuate lipopolysaccharide -stimulated neuroinflammation through NF-κB and p38 MAPK signaling pathways.
7. Glaucocalyxin A has inhibition of platelet aggregation, it can inhibit ADP- or arachidonic acid-induced platelet aggregation with IC50 values of 4.4 mumol/l,14.1 mumol/l respectively; it also can inhibit PAF-induced aggregation of rabbit platelets which were refractory to ADP and arachidonic acid with an IC50 value of 13.7 mumol/l.
8. Glaucocalyxin A may become a potential anti-fibrotic agent in Idiopathic pulmonary fibrosis (IPF) management, it can effectively ameliorate pulmonary fibrosis through the antagonism of leukocyte infiltration and proinflammatory cytokine production.