Salvianolic acid B

Salvianolic acid B is an active pharmaceutical compound present in Salvia miltiorrhiza, exerts a neuroprotective effect in animal models of brain and spinal cord injury.(In Vitro):Salvianolic acid B (SA-B) 1 and 10 micromol/L decrease the cell active TGF-beta1 secretion by 63.3 % and 15.6 % of the control, down-regulat pro-collgen alpha1(I) mRNA expression to 77.0% and 51.8% respectively (P<0.05). SA-B 1 and 10 micromol/L also inhibit MAPK activity by 1 to 2 fold respectively.The degradation of Salvianolic acid B is temperature dependent. It was stable at 4oC for 30 h in aqueous solution. However, decomposition of Salvianolic acid B aqueous solution occurres automatically at 25oC, and is enhanced at 37, 65 and 100oC. On the other hand, Salvianolic acid B is also stable at 4, 25 and 37oC for 30 h in TPA (total phenolic acids).Salvianolic acid B is stable for 30 h in buffered phosphate aqueous solutions at pH 1.5, 3.0 and 5.0. With an increase of pH from the neutral, the stability of Sal B decreased.\n(In Vivo):Salvianolic acid B (SalB) (5 mg · kg-1 · h-1) significantly attenuates LPS-induced pulmonary microcirculatory disturbance, including the increase in leukocyte adhesion and albumin leakage. In addition, LPS increases pulmonary tissue wet-to-dry weight ratio and tumor necrosis factor [alpha] and interleukin 8 levels in plasma and bronchoalveolar lavage fluid enhances the expression of E-selectin, intercellular adhesion molecule 1, myeloperoxidase, MMP-2, and MMP-9, whereas it decreases the expression of AQP-1 and AQP-5 in pulmonary tissue, all of which are attenuated by SalB pretreatment. SalB administration (10 mg/kg) significantly ameliorate the Aβ25-35 peptide-induced memory impairment in the passive avoidance task (P<0.05). SalB treatment also reduced the number of activated microglia and astrocytes that are observed during the inflammatory reaction after the administration of the Aβ25-35 peptide. Moreover, SalB markedly reduce inducible nitric oxide synthase and cyclooxygenase-2 expression levels and thiobarbituric acid reactive substances, which are increased by the administration of the Aβ25-35 peptide. Furthermore, SalB administration significantly rescue the Aβ25-35 peptide-induced decrease of choline acetyltransferase and brain-derived neurotrophic factor protein levels.