This study aims to investigate whether
escin ameliorates the impairments of neurological function by ameliorating systemic
inflammation instead of targeting the brain directly in
intracerebral hemorrhage (ICH) mice. It showed that
escin did not cross the blood brain barrier (BBB). Compared with the ICH group, the Garcia test scores in the
escin groups were significantly increased. Brain water contents and
Evans blue extravasation of the right basal ganglia in the ICH group were augmented, and significantly reduced by
escin.
Escin abated the increases of monocyte counts and serum IL-1β levels induced by ICH. IL-1β administration reversed the effect of
escin on Garcia test scores, the brain water contents, and the
Evans blue extravasation.
Escin ameliorated the increasing levels of RhoA, ROCK1, nuclear NF-κB and the decreasing expression of IκBα, cytosolic NF-κB,
occludin,
claudin-5 in the ICH group. IL-1β administration blocked not only
escin-mediated increases of IκBα, cytosolic NF-κB,
occludin, and
claudin-5, but also
escin-caused decreases of RhoA, ROCK1, and nuclear NF-κB. The results indicate that
escin improves neurological outcomes and the BBB function in ICH mice, which is associated with attenuating ICH-induced peripheral system
inflammation, and therefore, inhibiting IL-1β/RhoA/NF-κB signaling pathway in BBB, at least in part. These findings suggest that it may be useful to ameliorate
brain injury by inhibiting systemic
inflammation instead of aiming to target the brain directly after ICH.