ABSTRACT
Objective To investigate the expression of aquaporins 4 (AQP4) and histopathological changes in early phase of traumatic brain edema and the correlation between AQP4 expression and structural damage to blood-brain barrier (BBB).Methods A total of 120 healthy adult Wistar rats were divided into sham operation group and brain trauma group (which was subgrouped at hours 1,3,6,12 and 24 postinjury) according to random number table,with 20 rats per group.At each time point,brain water content was measured; brain edema and BBB structural changes were observed pathologically;IgG and AQP4 expressions in traumatic brain tissues were detected with immunohistochemical method and Western-blotting.Results In sham operation group,negatively stained IgG was observed and there were no abnormalities in brain tissue structure,brain water content as well as AQP4 expression.In brain trauma group,cerebral water content presented notable increase at 6 hours postinjury and peaked at 24hours; IgG expression showed significant increase at 1 hour postinjury,peaked at 6 hours postinjury and remained a high level at 24 hours.Pathologic observation revealed damage to BBB,blood red cells leaking out of the blood vessels,and tissue gap widening at 1 hour postinjury,which manifested as vasogenic brain edema.Further,those phenomena were gradually aggravated over time and became obvious at 6 hours postinjury.Intracellular edema occurred at 3 hours postinjury,with the presence of increased glial cell body,cytoplasm light staining or vacuolar degeneration,as well as mitochondria swelling and was also aggravated with time,particularly at 6 hours postinjury.Except that the previously mentioned two forms of edema coexisted at 12 hours postinjury,tissue necrosis,inflammatory cell infiltration and microglia proliferation were emerged and aggravated at 24 hours postinjury.AQP4 level decreased at 1 hour,minimized at 6 hours and regained at 12 hours,showing a V-shape curve.Conclusions Vasogenic edema characterized by BBB disruption is the primary histopathological change in early-phase of brain trauma,followed by the coexistence with intracellular edema and aggravation of the two forms of edema over time.AQP4 expression is down-regulated in the vasogenic edema phase but highly expressed at phase of the intracellular edema.
ABSTRACT
Objective To study the expression of aquaporins-4 (AQP4) in the brain tissue of rats with pancreatic encephalopathy (PE) induced by phospholipase A2 and to explore the role of aquaporins-4 in PE.Methods Twenty five healthy Wistar rats were randomized into 3 groups:blank group ( n =5),PE group (n =10 ) and control group (n =10 ).The experimental model was established in rats by injecting phospholipase A2 into carotid artery (0.1 ml/100 g body weight).Same amount of normal saline was used in the control group and no treatment was used in the blank group.One day later,the rats were sacrificed,then the measurement of brain tissue wet/dry (W/D) weight ratio was performed,and brain tissue was routinely pathologically examined,immunohistochemistry and Western blotting were performed in each group to detect the expression of aquaporins-4.Results There was no obvious brain tissue pathological change in the control group and blank group.Neurons in the brain tissue of PE rats presented with significant edema and ballooning degeneration,infiltration of inflammatory cells,leukocyte aggregation around the microvessels.The water contents in the brain tissue in the blank group and control group,PE group were (61.44 ±0.36)％,(63.20±0.32)％ and (78.33 ±0.24)％,and it was significantly higher in PE group than that in the control and blank group (P＜0.05).The expressions of aquaporins-4 in the brain tissue were 0.41 ±0.27,0.49 ±0.13,0.98 ±0.21,respectively,and it was significantly increased in PE group than that in the control and blank group (P ＜ 0.05 ).Conclusions Aquaporins-4 may play important roles in the pathogenesis of pancreatic encephalopathy.