Bo Chen,Kai Sun,Yu-Ying Liu,Xiang-Shun Xu,Chuan-She Wang,Ke-Seng Zhao,Qiao-Bing Huang,Jing-Yan Han.[J].Chin J Traumatol,2016,19(2):85-93. [doi]
Effect of salvianolic acid B on TNF-a induced cerebral microcirculatory changes ina micro-invasive mouse model
  
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KeyWord: MicrocirculationTumor necrosis factor-alphaSalvianolic acid B
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Author NameAffiliation
Bo Chen Department of Pathophysiology, Key Laborotory for Shock and Microcirculation Research, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China 
Kai Sun Tasly Microcirculation Research Center, Health Science Center, Peking University, Beijing, China 
Yu-Ying Liu Tasly Microcirculation Research Center, Health Science Center, Peking University, Beijing, China 
Xiang-Shun Xu Tasly Microcirculation Research Center, Health Science Center, Peking University, Beijing, China 
Chuan-She Wang Tasly Microcirculation Research Center, Health Science Center, Peking University, Beijing, China 
Ke-Seng Zhao Department of Pathophysiology, Key Laborotory for Shock and Microcirculation Research, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China 
Qiao-Bing Huang Department of Pathophysiology, Key Laborotory for Shock and Microcirculation Research, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China 
Jing-Yan Han Department of Integration of Chinese and Western Medicine, School of Basic Medical Sciences, Peking University, Beijing 100083, China 
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Abstract:
      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 mg/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 CD11b/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 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 CD11b/CD18 and CD62L in leukocytes and E-selectin and ICAM-1 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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