Effect of salvianolic acid B on TNF-a induced cerebral microcirculatory changes in a micro-invasive mouse model
Effect of salvianolic acid B on TNF-a induced cerebral microcirculatory changes in a micro-invasive mouse model作者机构：Department of Pathophysiology Key Laborotoryfor Shock and Microcirculation Research School of Basic Medical Sciences Southern Medical University Guangzhou 510515 China Tasly Microcirculation Research Center Health Science Center Peking University Beijing China Department of Integration of Chinese and Western Medicine School of Basic Medical Sciences Peking University Beijing 100083 China
出 版 物：《Chinese Journal of Traumatology》 (中华创伤杂志（英文版）)
年 卷 期：2016年第19卷第2期
页 面：85-93页
核心收录：
学科分类：0403[教育学-体育学] 1002[医学-临床医学] 100204[医学-神经病学] 10[医学]
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
主 题：MicrocirculationTumor necrosis factor alphasalvianolic acid B
摘 要：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/*** 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.
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