Investigating the effect of HS on up-regulation of brain AQP4 during LPS-induced mice brain edema would provide clues to reveal the mechanism of HS down-regulation of brain AQP4 in bacterial meningitis.
AQP4-null mice showed better survival rates compared to wild-type mice in the brain edema model caused by acute water intoxication, or focal ischemic stroke by cerebral artery occlusion (Manley et al. 2000).
The expression of AQP4 is up-regulated in wild type mice and AQP4 null mice have significantly less brain edema in water intoxication cerebral edema, ischemic stroke and pneumococcal meningitis [ 23, 24].
Accordingly, Vasp−/− mice developed significantly more brain edema (0.8 mm3±0.4 mm3 versus 1.7 mm3±0.5 mm3, respectively; p<0.0001).
To assess whether the reduction in early brain injury and the improvement of neurologic deficits in EC-treated micorrelatedted with reduced brain edema, we examined brain water content 72 h after ICH.
Some viruses are also known to infect mouse brain endothelial cells, increasing CNS vascular permeability and resulting in edema and an increased local viral load [44], [45].
AQP4 null mice have lower mortality and are less prone to cytotoxic brain edema, including water intoxication cerebral edema [ 23], early focal cerebral ischemia [ 23] and bacterial meningitis [ 24].
Recent studies in the AQP4 knockout or overexpressing mice demonstrated a dual role for AQP4 in the pathophysiology of brain edema [1], [3], [4], [5], [6], [7].
It is noteworthy that AQP4 mislocalization in these mice results in a better outcome as it delays the onset of brain edema [32], [40].
CLP mice showed obvious brain injury characterized by aggravated pathological damage, BBB disruption and brain edema at 24 h after CLP operation, which was markedly alleviated by 2% H2 treatment.
