Excess salt exacerbates blood-brain barrier disruption via a @entity1435 /MAPK/ @entity15188 -dependent pathway in permanent XXXX .

@entity1 @entity455 @entity64 @entity101 @entity2806 @entity63 @entity19 @entity75 @entity1372 @entity15188 @entity1702 @entity1435 @entity2827 @entity4202 @entity385
@entity1702 ( @entity1702 ) is one of the most important risk factors that contribute to many @entity455 including @entity385 . One proposed mechanism underlying the disruption of blood-brain barrier (BBB) mediated by @entity1702 is indirectly through enhancing blood pressure. The direct role of @entity1702 on BBB integrity is unclear. Our purpose is to determine whether and how @entity1702 might be involved in BBB breakdown during @entity63 . To test that, we induced model of @entity2806 by permanent middle cerebral artery ligation (pMCAL) in either normal diet or @entity1702 fed @entity19 . We observed that @entity1702 significantly enhanced @entity63 @entity75 which was associated with enhanced BBB disruption, increased leukocytes infiltration and loss of tight junction (TJ) proteins expression without apparently altering blood pressure. Our in vitro experiment also revealed that @entity2827 ( @entity4202 ) treatment down-regulated TJ protein expression by endothelial cells and substantially increased BBB permeability during starvation. Inhibition of @entity1435 /MAPK/ @entity15188 pathway eliminated the effect of @entity4202 on BBB permeability in vitro. In addition, we noticed a positive correlation between urinary @entity1372 levels and @entity63 lesion size in @entity64 @entity1 . Together, our study demonstrates a @entity101 -independent role of @entity1702 during @entity63 and provides rationale for post cerebral @entity63 management.
