Effect of salvianolic acid B on TNF-α induced cerebral microcirculatory changes in a micro-invasive mouse model.
- Author:
Bo CHEN
1
;
Kai SUN
;
Yu-Ying LIU
;
Xiang-Shun XU
;
Chuan-She WANG
;
Ke-Seng ZHAO
;
Qiao-Bing HUANG
;
Jing-Yan HAN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Benzofurans; pharmacology; Blood Flow Velocity; Cerebrovascular Circulation; drug effects; Craniotomy; Disease Models, Animal; E-Selectin; metabolism; Intercellular Adhesion Molecule-1; metabolism; Mice; Mice, Inbred C57BL; Microcirculation; drug effects; Random Allocation; Reference Values; Tumor Necrosis Factor-alpha; administration & dosage
- From: Chinese Journal of Traumatology 2016;19(2):85-93
- CountryChina
- Language:English
-
Abstract:
PURPOSETo investigate the effects of salvianolic acid B (SAB) on tumor necrosis factor a (TNF-α) induced alterations of cerebral microcirculation with a bone-abrading model.
METHODSThe 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. Immunohistochemical staining was also used to detect E-selectin and ICAM-1 expression in endothelial cells.
RESULTSCompared 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 CD11b/CD18 and CD62L in leukocytes and E-selectin and ICAM-1 in endothelial cells induced by TNF-α.
CONCLUSIONSThe 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.