Changes in aquaporin 4 expressions in the brain tissues of rats with streptococcus pneumoniae meningitis / 中华实用儿科临床杂志

ABSTRACT

Objective To investigate the expressions of aquaporin 4 (AQP4) in the bacterial meningitis in rats and to explore the molecular mechanism for brain edema caused by bacterial meningitis.Methods Totally 40 of 3-week-old-Sprague-Dawley healthy rats,body weight 60-80 g,male or female,were divided into a normal control group(n =10),and infection groups24 hours after injection(n =10),48 hours after injection(n =10),and 5 days after injection(n =10).The expressions of AQP4 in the brain were detected by immunohistochemistry and Western blot methods respectively after 24 hours,48 hours,5 days of inoculation.Results Mortality rateno rats in the control group and the infection group after 24 hours were dead.Two rats in the infection group after 48 hours and 4 rats in the infection group after 5 days were dead because of serious sickness,with the mortality rates 20％ and 40％,respectively.AQP4 expression was slightly positive under light microscope,and the positive cells mainly surrounded glial cells and blood vessels,while neurons were not dyed.Immunohistochemical staining showed that AQP4 expression in the model group increased with the severity of edema;compared with the control group,the AQP4 expression in the brain tissues increased in different periods after rats were infected,and the differences between groups were statistically significant (F--91.84,P ＜ 0.01).Western blot analysis showed that after the brain received streptococcus pneumoniae injection,expression of AQP4 began to increase in 24 hours after streptococcal injection,and reached to the peak in 48 hours,but decreased in 5 days,but the expression still remained higher than that of the normal control group.Each group had statistically significant difference(F =14.23,P ＜ 0.01).Conclusions Expression of AQP4 in the models with bacterial meningitis may increase initially and decrease later.It suggests that AQP4 plays a protective role during the development of infectious brain edema.