Cyclobuxine D is a steroidal alkaloid extracted from Buxus microphylla. Cyclostatin D has obvious bradycardia effect on rat heart, and inhibits acetylcholine and Ba ++ induced longitudinal muscle contraction isolated from rabbit jejunum.
C19 Ceramide is a naturally occurring ceramide that has been found in J. juncea extracts as well as rat brain and mouse heart.[1],[2],[3] It is elevated in adult and decreased in juvenile whole rat brain extracts by 114 and 37%, respectively, following chronic ethanol exposure.[2] C19 Ceramide is also increased in mouse hearts following administration of angiotensin II.[3]
(3S)-hydroxy Quinidine is an active quinidine metabolite. Quinidine, an antiarrhythmic agent, undergoes rapid first-pass metabolism by the cytochrome P450 (CYP) isoforms CYP3A4, CYP2C9, CYP2E1, and CYP3A5, with CYP3A4 being the most active enzyme in the (3S)-hydroxy quinidine formation. (3S)-hydroxy Quinidine prolongs repolarization of canine Purkinje fibers in vitro and prevents ventricular fibrillation and ventricular tachycardia after coronary reperfusion in isolated rat hearts in a dose-dependent manner.
[D-Trp11]-Neurotensin is a compound that functions as a selective antagonist of Neurotensin (NT) in perfused rat hearts, while exhibiting full agonist properties in guinea pig atria and rat stomach strips. Additionally, this compound can inhibit hypotension induced by NT.
L-2286 is a novel PARP inhibitor. L-2286 exerted significant protective effect against ischemia-reperfusion-induced myocardial injury in both experimental models. More importantly, L-2286 facilitated the ischemia-reperfusion-induced activation of Akt, extracellular signal-regulated kinase, and p38-MAPK in both isolated hearts and in vivo cardiac injury.