[CAS NO. 121521-90-2]  Salvianolic acid B

Salvianolic 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 mg/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)