Purpose： To investigate the effects of salvianolic acid B （SAB） on tumor necrosis factor a （TNF-a） induced alterations of cerebral microcirculation with a bone-abrading model. Methods： The influences of cranioto...Purpose： To investigate the effects of salvianolic acid B （SAB） on tumor necrosis factor a （TNF-a） induced alterations of cerebral microcirculation with a bone-abrading model. Methods： The influences of craniotomy model and bone-abrading model on cerebral microcirculation were compared. The bone-abrading method was used to detect the effects of intracerebroventricular application of 40 μg/kg.bw TNF-a on cerebral venular leakage of fluorescein isothiocyanate （FITC）- albulmin and the rolling and adhesion of leukocytes on venules with fluorescence tracer rhodamine 6G, The therapeutical effects of SAB on TNF-a induced microcirculatory alteration were observed, with continuous intravenous injection of 5 mg/kg.h SAB starting at 20 min before or 20 min after TNF-a administration, respectively, The expressions of CDllb/CD18 and CD62L in leukocytes were measured with flow cytometry, Immunohistochemical staining was also used to detect E-selectin and ICAM-1 expression in endothelial cells, Results： Compared with craniotomy method, the bone-abrading method preserved a higher erythrocyte velocity in cerebral venules and more opening capillaries. TNF-a intervention only caused responses of vascular hyperpermeability and leukocyte roiling on venular walls, without leukocyte adhesion and other hemodynamic changes. Pre- or post-SAB treatment attenuated those responses and suppressed the enhanced expressions of CDII b/CDI8 and CD62L in leukocytes and E-selectin and ICAM-I in endothelial cells induced by TNF-a. Conclusions： The pre- and post-applications of SAB during TNF-a stimulation could suppress adhesive molecular expression and subsequently attenuate the increase of cerebral vascular permeability and leukocyte rolling.展开更多
OBJECTIVE:To investigate the influence and mechanism of salvianolic acid B(SalB) on apoptosis inhibition in rat bone marrow-derived mesenchymal stem cells(BMSCs) induced by hypoxia and serum deprivation(hypoxia/SD).ME...OBJECTIVE:To investigate the influence and mechanism of salvianolic acid B(SalB) on apoptosis inhibition in rat bone marrow-derived mesenchymal stem cells(BMSCs) induced by hypoxia and serum deprivation(hypoxia/SD).METHODS:SalB concentration of 0.1,1,10 or 100 mg/L(drug groups) were investigated for their ability to inhibit apoptosis in rat BMSCs.BMSCs in both the apoptosis model and drug groups were cultured under hypoxic conditions for 6 h,after which cell apoptosis and change in mitochondrial membrane potential(MMP) were detected using flow cytometry.Activation of caspase-3 was detected using western blot analysis.RESULTS:Hypoxia/SD induced apoptosis in rat BMSCs.The early apoptosis rate was lower in the drug groups compared to the apoptosis model group(P<0.05).SalB was found to inhibit the reduction in MMP and decrease the activation of caspase-3.CONCLUSION:0.1,1 and 10 mg/L of SalB inhibits activation of caspase-3 and early apoptosis of rat BMSCs induced by hypoxia/SD and could therefore enhance the survival rate of grafted stem cells.展开更多
基金This study was supported by the General Program from the Natural Science Foundation of China，Southern Medical University Research Program for Young Scientists Training
文摘Purpose： To investigate the effects of salvianolic acid B （SAB） on tumor necrosis factor a （TNF-a） induced alterations of cerebral microcirculation with a bone-abrading model. Methods： The influences of craniotomy model and bone-abrading model on cerebral microcirculation were compared. The bone-abrading method was used to detect the effects of intracerebroventricular application of 40 μg/kg.bw TNF-a on cerebral venular leakage of fluorescein isothiocyanate （FITC）- albulmin and the rolling and adhesion of leukocytes on venules with fluorescence tracer rhodamine 6G, The therapeutical effects of SAB on TNF-a induced microcirculatory alteration were observed, with continuous intravenous injection of 5 mg/kg.h SAB starting at 20 min before or 20 min after TNF-a administration, respectively, The expressions of CDllb/CD18 and CD62L in leukocytes were measured with flow cytometry, Immunohistochemical staining was also used to detect E-selectin and ICAM-1 expression in endothelial cells, Results： Compared with craniotomy method, the bone-abrading method preserved a higher erythrocyte velocity in cerebral venules and more opening capillaries. TNF-a intervention only caused responses of vascular hyperpermeability and leukocyte roiling on venular walls, without leukocyte adhesion and other hemodynamic changes. Pre- or post-SAB treatment attenuated those responses and suppressed the enhanced expressions of CDII b/CDI8 and CD62L in leukocytes and E-selectin and ICAM-I in endothelial cells induced by TNF-a. Conclusions： The pre- and post-applications of SAB during TNF-a stimulation could suppress adhesive molecular expression and subsequently attenuate the increase of cerebral vascular permeability and leukocyte rolling.
基金Supported by China Post-doctoral Scientific Fund (20090450542)
文摘OBJECTIVE:To investigate the influence and mechanism of salvianolic acid B(SalB) on apoptosis inhibition in rat bone marrow-derived mesenchymal stem cells(BMSCs) induced by hypoxia and serum deprivation(hypoxia/SD).METHODS:SalB concentration of 0.1,1,10 or 100 mg/L(drug groups) were investigated for their ability to inhibit apoptosis in rat BMSCs.BMSCs in both the apoptosis model and drug groups were cultured under hypoxic conditions for 6 h,after which cell apoptosis and change in mitochondrial membrane potential(MMP) were detected using flow cytometry.Activation of caspase-3 was detected using western blot analysis.RESULTS:Hypoxia/SD induced apoptosis in rat BMSCs.The early apoptosis rate was lower in the drug groups compared to the apoptosis model group(P<0.05).SalB was found to inhibit the reduction in MMP and decrease the activation of caspase-3.CONCLUSION:0.1,1 and 10 mg/L of SalB inhibits activation of caspase-3 and early apoptosis of rat BMSCs induced by hypoxia/SD and could therefore enhance the survival rate of grafted stem cells.
