Molecular Formula | C36H30O16
|
Molar Mass | 718.61 |
Density | 1.637±0.06 g/cm3(Predicted) |
Melting Point | 98-110°C |
Boling Point | 1020.3±65.0 °C(Predicted) |
Flash Point | 322.1°C |
Solubility | H2O: ≥5mg/mL |
Vapor Presure | 0mmHg at 25°C |
Appearance | powder |
Color | white to tan |
pKa | 2.77±0.10(Predicted) |
Storage Condition | -20°C |
Refractive Index | 1.739 |
Physical and Chemical Properties | From the Labiatae plant salvia miltiorrhiza (Savia miltiorrhiza) |
In vitro study | Salvianic acid B (also known as satanic acid B or lithospermic acid B) is a new generation of natural antioxidants. It can affect the NO release of endothelial cells induced by hypoxia/reoxygenation and affect the accumulation of calcium ions. When acid B was treated at a concentration of 2.5, 5, and 10 mg/l, cell viability and SOD activity were enhanced and malondialdehyde formation in human umbilical vein endothelial cells (ECV304) was inhibited. SalB inhibited high glucose-induced oxidative stress in a dose-dependent manner and reduced the production of ROS and 8-OHDG, mitochondrial depolarization and apoptosis. It can down-regulate the expression of Bax and nuclear translocation of AIF, and the release of cytochrome c mediated by high glucose; Up-regulate the expression of Bcl-2 induced by high glucose (HG). In addition, SalB attenuates HG-induced caspase-3, -9, and reduces PARP division in Schwann cells. SalB inhibited the gelatinolytic activity induced by angiotensin II or H2O2 and TNF-α in human aortic smooth muscle cells in a concentration-dependent manner. Salvianic acid B inhibits platelet aggregation and adhesion and promotes cardiovascular Genesis. SalB also enhances cell viability, reduces the number of ischemic cells in the sub-G1 phase, and resists apoptosis. It can inhibit the effects of ischemia and hypoxia in myocardial injury. Inhibition of type I collagen synthesis in a non-TGF-1 stimulated human hepatic stellate cell line (LX-2). SalB activates mammalian SIRT1 (a NAD-dependent type of histone deacetylase). |
In vivo study | Salvianic acid B can significantly reduce the infarct size and blood lactate dehydrogenase level, improve cardiac function and myocardial tissue structure in the rat model of acute myocardial infarction, thus inhibiting myocardial ischemia and hypoxia injury. Salvianic acid B also improves blood rheology, reduces oxidative damage, improves vascular endothelial cell function and prevents the development of coronary artery disease. In the rat model of myocardial infarction, SalB can selectively inhibit the activity of MMP-9, effectively increase the thickness of the left ventricular wall, improve the contractility of the heart, and reduce myocardial fibrosis. SalBd can attenuate ethanol-induced liver inflammation, mainly by reducing the expression levels of hepatotoxic cytokines such as TNF-α and IL-6. In animal models, SalB has been shown to be effective in the treatment of hepatic fibropathy, while exerting cardioprotective and neuroprotective activities through its antioxidant and anti-inflammatory activities. |