Salvianolic acid B (C09-1043-790)

InformationSalvianolic acid B Salvianolic acid B (Sal B, Lithospermate B, Lithospermic acid B), an antioxidant and free radical scavenging compound, is the most abundant bioactive compound extracted from the root of Salvia miltiorrhiza Bunge.In vitroSalvianolic acid B, also known as satanic acid B or lithospermic acid B, is a new generation of the natural antioxidants. It can influence Ca2+ aggregation and endothelial cell NO release of hypoxia/ reoxygenation-induced cell. When acid B concentration is 2.5, 5, and 10/u2009mg/l, cell viability and superoxide dismutase (SOD) activity are enhanced, and the formation of malondialdehyde (MDA) in human umbilical vein endothelial cells (ECV304) is inhibited. SalB inhibits HG-induced oxidative stress and reduces the generation of ROS and 8-hydroxy-2-deoxyguanosine (8-OHDG) and mitochondrial depolarization and apoptosis in a dose-dependent manner. It can downregulate the expression of Bax and AIF nuclear translocation and cytochrome c release mediated by HG, but upregulate the expression of Bcl-2 induced by HG. Besides, SalB attenuates HG-induced caspase of the enzyme 3, 9 and minimize PARP cleavage of Schwann cells (SCs). SalB inhibits angiotensin II or H2O2 and TNF-α-induced gelatinolytic activity in human aortic smooth muscle cells (HASMCs) in a concentration-dependent manner. Salvianolic acid B can inhibit platelet aggregation and adhesion. Salvianolic acid B can promote cardiac angiogenesis effect. SalB can enhance cell activity and reduce the number of sub-G1 and apoptotic nuclei of ischemic cell model in order to show its antiapoptotic effects. Salvianolic acid B inhibits ischemia and hypoxia of myocardial injury. Salvianolic acid B inhibits the synthesis of type I collagen of non-TGF-1 stimulated human hepatic stellate cell line (LX-2). SalB activates mammalian sirtuins 1 (SIRT1), an NAD-dependent class III histone deacetylase (HDAC) that plays important roles in several physiological processes, including gene transcription, senescence, energy metabolism, oxidative stress and inflammation. (HG：High glucose)In vivoSalvianolic acid B can significantly reduce the myocardial infarct size and blood lactate dehydrogenase level of model rat with acute myocardial infarction, improve cardiac function and myocardial tissue structure, thus inhibiting ischemia and hypoxia of myocardial injury. salvianolic acid B can improve blood hemorheology, reduce oxidative damage, improve the vascular endothelial cell function, and prevent the development of coronary artery disease. Salvianolic acid B could selectively inhibit the activity of MMP-9 in a rat model of myocardial infarction. Salvianolic acid B can also effectively increase the thickness of the left ventricular wall in the myocardial infarction rats to improve the contraction of the heart, and reduce cardiac fibrosis. SalB treatment ameliorates ethanol-induced hepatic inflammation by decreasing the levels of hepatotoxic cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). SalB has beneficial effects against hepatic fibrosis in animal models and has been shown to possess cardioprotective and neuroprotective activity via anti-oxidative and anti-inflammatory actions.Cell Datacell lines：Concentrations：8 μMIncubation Time：3 hPowder Purity:≥98%. Specification: 10mM in DMSO Molecular Formula: C36H30O16 Molecular Weight: 718.61