Increased activity of Rho kinase contributes to hemoglobin-induced early disruption of the blood-brain barrier in vivo after the occurrence of XXXX .

@entity22677 @entity13291 @entity6929 @entity35 @entity20757 @entity1779
This study is to examine whether the activation of Rho kinase (ROCK) accounts for hemoglobin (Hb)-induced disruption of blood-brain barrier (BBB) after the occurrence of @entity1779 . A model of intracerebral injection of Hb was established in @entity35 . Changes in the levels of mRNA of @entity20757 , @entity13291 and @entity6929 ( @entity6929 ) were measured using quantitative real-time polymerase chain reaction. Protein expression of @entity20757 , @entity13291 , @entity22677 and @entity6929 , as well as ROCK activity, were determined using Western blotting. Immunohistochemical assay was performed to visualize the expression of @entity20757 , @entity13291 , @entity22677 and @entity6929 in endothelial cells. Hb injection produced a significant increase in BBB permeability and water content in the brain. Significant reduction of @entity22677 expression was detected by Western blotting and immunofluorescence in Hb group. The levels of @entity20757 and @entity13291 were significantly up-regulated from 6 h to 12 h after Hb injection and were concomitant with the increase in ROCK activity. Immunofluorescence double staining showed enhanced p-myosin light chain immunoreactivity but diminished @entity22677 staining in endothelial cells. Significant up-regulation of @entity6929 expression was detected after Hb injection, and statistical analyses further confirmed a positive correlation of @entity6929 expression with ROCK activity. The results showed that ROCK was activated in endothelial cells by Hb. This may account for the early disruption of the BBB via up-regulation of p-myosin light chain expression and aggravation of injuries to TJ proteins. The activation of ROCK may also increase @entity6929 expression, thereby leading to further BBB disruption.
