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Salvianolic acid B

  Cat. No.:  DC5998   Featured
Chemical Structure
121521-90-2
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More than 5000 active chemicals with high quality for research!
Field of application
Salvianolic acid B is a cell protective antioxidant and free radical scavenger being investigated for a variety of conditions from ischemic heart disorders to Alzheimer′s disease.
Chemicals PropertiesBiological activity COA & MSDSRelated productsDatasheet
Cas No.: 121521-90-2
SMILES: C1=CC(=C(C=C1C[C@H](C(=O)O)OC(=O)/C=C\C2=C3[C@H]([C@@H](OC3=C(C=C2)O)C4=CC(=C(C=C4)O)O)C(=O)O[C@H](CC5=CC(=C(C=C5)O)O)C(=O)O)O)O
Formula: C36H30O16
M.Wt: 718.63
Purity: >98%
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: Salvianolic acid B is an active ingredient of Salvia miltiorrhiza, which has been widely applied in China for the management of various microcirculation-related disorders, such as cardiovascular disease, cerebrovascular disease, and diabetic vascular complication.
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[1]. 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[2].
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 [3].
References: [1]. Lee YW, et al.Neuroprotective effects of salvianolic acid B on an Aβ25-35 peptide-induced mouse model of Alzheimer's disease. Eur J Pharmacol. 2013 Mar 15;704(1-3):70-7. [2]. Liu P, et al. Effect of salvianolic acid B on collagen production and mitogen-activated protein kinase activity in rat hepatic stellate cells. Acta Pharmacol Sin. 2002 Aug;23(8):733-8. [3]. Lin, Fang, et al. Salvianolic acid B protects from pulmonary microcirculation disturbance induced by lipopolysaccharide in rat. Shock. 2013 Mar;39(3):317-25.
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
2018-0101
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