ABSTRACT
In this paper, human umbilical vein endothelial cells (HUVEC) hypoxic injury models were established by sodium dithionite (Na2S2O4). With the protective effects of total salvianolic acids components (TSAC) against oxidative damage of HUVEC as a starting point, cellviability was measured by MTT colorimetric method； intracellular superoxide dismutase (SOD) activity, malondialdehyde (MDA), lactatedehydrogenase (LDH) level, nitric oxide (NO) level, interleukin6 (IL-6), and human tumor necrosis factor α (TNF-α) expression were measured by kits, to investigate the effect of seven kinds of phenolic acids of TSAC on Na2S2O4-induced HUVEC hypoxic injury. Based on the "component structure" theory, the contribution of the main components in TSAC for the protective effect on hypoxic injury of HUVEC was studied. The results showed that salvianolic acid B, posrnarinic acid A, salvianolic acid A, lactic acid, and lithospermic acid in TSAC play a larger role in protective effect of hypoxic injury of HUVEC. These five components were administered in combinations respectively, and it was concluded that the four components including salvianolic acid B, posrnarinic acid A, salvianolic acid A, lactic acid could be used as the representative components of TSAC.
ABSTRACT
Objective: To establish a blood-brain barrier (BBB) model for screening the effective ingredients of total salvianolic acids components probably effecting central nervous system (CNS), so as to provide basis for the rapid high throughput screening of CNS drugs. Methods: The permeability parameters and transendothelial electrical resistance (TEER) values showed that the co-cultured human brain microvascular endothelial cells (HBMEC)/HA (human astrocytes) model was of integrity and vitality. The active components in total salvianolic acids were screened with this in vitro BBB model, and then analyzed by HPLC-MS. Results: HA induced HBMEC to produce higher TEER in the first 10 d up to 300 Ω/cm2, sodium fluorescein was used to detect the formation of tight junctions of endothelial cells, and the permeability coefficient of its cross-vitro BBB model was (2.659 ± 0.730) × 10-3 cm/min. We found that six compounds at least from total salvianolic acids could permeate across BBB model, in which danshensu, protocatechuic acid, caffeic acid, isoferulic acid, lithospermic acid, and rosmarinicacid were identified. Conclusion: The co-cultured HBMEC/HA model combined with HPLC-MS analysis is a potential tool for screening of BBB permeable drug candidates from plant-derived materials.
ABSTRACT
Aim The protective effect of total salvianolic acids (Sal) on cerebral hypoxia inmice was studied. Methods Acute cerebral hypoxia was induced by sodium nitrite scand decapitation.The effect of Sal on acute cerebral hypoxia in mice and neuronalhypoxia injury induced by sodium dithionite in primary cultures were ob-served. Results Sal in the doses of 10, 20 mg?kg-1 iv protected mice against theacute cerebral hypoxia and inhibited the production of lipid peroxidation in brain tis-sue of mice caused by cerebral hypoxia. Sal in the doses of 1~10 ?g? L-1 reduced therate of cell death and the content of MDA and lowered LDH content in extra-cellularbathing media in oxygen deprived cortical cultures.Conclusions Sal protects miceagainst cerebral hypoxia by suppressing the generation of lipid peroxide.
ABSTRACT
Object It was reported that salvianolic acid A from Salvia miltiorrhiza Bge could improve memory dysfunction of mice with cerebral ischemia reperfusion injury The effects of total salvianolic acids (Sal), including salvianolic acid A and B, rosmaric acid and protocatechic aldehyde was now studied to observe its effect on cerebral ischemia reperfusion injury in hope of obtaining a preliminary view on its mechanism of action Methods The effects of Sal on lactic dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA) of cerebral ischemia reperfusion injured mouse and rat models were observed Results Sal 10, 20 mg/kg iv and 5, 10 mg/kg iv could markedly increase the activities of LDH and SOD and lower the production of MDA in the injured cerebral tissue On focal cerebral ischemia reperfusion injured rat, 24 h reperfusion after 2 h ischemic injury, 5, 10 mg/kg iv Sal could decrease infarct size, ameliorate neurological deficit with obvious inhibition of the decrease of LDH and SOD activities and the over production of MDA Conclusion Sal showed obvious protective effects on cerebral ischemia reperfusion injuries of mice and rats via attenuating oxygen free radical