Aquaporin-4 expression in developing rat brain following status epilepticus (SE) and the effects of exogenous GM1 on it

Objectives: The aim of study was to investigate the relationship between aquaporin-4 (AQP4) and brain edema following status epilepticus (SE) via observing the changes of AQP4 expression in brain edema formation following SE in the developing rats, We also observed the effects of Monosialote-trahexosylganglioside (GM1) on the expression of AQP4 and brain edema following SE, contributing to learn more about the protective function of GM1 on brain edema due to SE. Methods: One hundred and fifty male developing Spraque-Dawley (SD) rats were randomly divided into three groups: control group, status epilepticus group (SE group) which was induced by pilocarpine (PILO), and GM1 group (SE+GM1), in which the rats were given intraperitoneal injection of GM1 30 mg/kg after SE, once again every 24 h for six times. Each group was subjected to 4 subgroups: 6 h, 24 h, 72 h and 7 d after SE (n= 5). Each brain tissue was respectively used to observe the changes of morphology, to determine the brain water content (BWC) by brain wet-to-dry weight ratio and to determine the expression of AQP4 by using immunohistochemical staining and to be semi quantified as an optical density (OD) value of positive cells with pathology imaging analysis system (PIAS). Results: In control group, there were no significant changes of the morphology, both the brain water content and the expression of AQP4. In SE group, HE staining showed swelling, degeneration of the brain cell and proliferation of astrocyte, so did the changes of SE+GM1 group. Compared with control, SE group significantly increased BWC and the expression of AQP4, all began at 6 h and peaked at 72 h (P<0.05), but no variance at 7 d (P>0.05). AQP4 expression positively correlated with BWC (r=0.623, P< 0.01). In SE+GM1 group, compared with SE group, the elevation of BWC was strongly attenuated at all time point except 7 d. While AQP4 levels demonstrated an obviously atenuation from 24 h. At 72 h, the AQP4 OD value decreased from 0.396 +/- 0.026 (SE group) to 0.243 +/- 0.036 (SE+GM1 group_) (P<0.05). Conclusions: Cerebralcortical AQP4 expression is up-regulated after SE with the deterioration of brain edema. It reveals that AQP4 participates in the development of brain edema after SE. Exogenous GM1 may inhibit AQP4 expression after SE and attenuate brain edema.