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Purpose:To investigate the effects of salvianolic acid B (SAB) on tumor necrosis factor α (TNF-α) 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-α 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-α 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-α administration,respectively.The expressions of CD11b/CD18 and CD62L in leukocytes were measured with flow cytometry.lmmunohistochemical 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-α intervention only caused responses of vascular hyperpermeability and leukocyte rolling on venular walls,without leukocyte adhesion and other hemodynamic changes.Pre-or post-SAB treatment attenuated those responses and suppressed the enhanced expressions of CD11 b/CD18 and CD62L in leukocytes and E-selectin and ICAM-1 in endothelial cells induced by TNF-α.Conclusions:The pre-and post-applications of SAB during TNF-α stimulation could suppress adhesive molecular expression and subsequently attenuate the increase of cerebral vascular permeability and leukocyte rolling.