Expression and roles of aquaporin 1 in hippocampus of mice model with traumatic brain injury

Chinese Journal of Contemporary Neurology and Neurosurgery

Bo QIU¹  Yun-jie WANG¹  Yong WANG¹  Xin-guo LI¹  Jun WANG¹ 

[1] Department of Neurosurgery, the First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning, China;

关键词: Brain injuries;    Aquaporins;    Hippocampus;    Brain edema;    Apoptosis;    Immunohistochemistry;    Immunoblotting;    Disease models, animal;   

DOI  :  

来源: DOAJ

【 摘 要 】

Background The "secondary brain insult" including ischemia,hypoxia and edema after primary traumatic brain injury (TBI) may deteriorate thebrain damages and greatly influence the prognosis. As a selective vulnerableregion, the hippocampus is especially sensitive to ischemia, hypoxia or edemaand yields irreversible sequelae. Aquaporin 1 (AQP1) has been reported to berelated to cerebral edema, but the expression and role of AQP1 in hippocampaledema after TBI have seldomly been investigated. In this study, we establishedBALB/c mouse closed craniocerebral injury models and investigated the changes ofAQP1 expression in hippocampus of mouse models after TBI, thereby discussing itseffects on relevant pathophysiological processes.  Methods Seventy-five BALB/c mice were used to establish experimental closed TBI modelswith a free-falling weight drop device, and the equal numbers of mice weresubject to sham operation and categorized as sham group. The neurologicalfunction of each mouse in either TBI group or sham group was scored at differenttime points (1, 6, 24 and 72 h) after TBI or sham operation, and brain edemaformation of the mice in both groups was also evaluated accordingly at 6, 24 and72 h. The apoptotic hippocampal cells were stained in situ and detected usingTdT-mediated dUTP-biotin nick end labeling (TUNEL) method at different timepoints (6, 24 and 72 h), then AQP1 expression in hippocampus was alsocorrespondingly detected using immunohistochemistry and Western blotting. Allthe data were finally compared with those in sham operation group and analyzed. Results Experimental TBI models were successfully establishedand confirmed by the neurological function score and hippocampal edemaevaluation. Six hours after craniocerebral injury, the apoptotic cells increasedsignificantly in the hippocampus of mice in TBI group compared with those insham group [(44.26 ± 15.18)% vs (8.61 ± 8.25)% , t = - 9.676,P = 0.002]. The apoptotic rate increased gradually with the prolongingof time and was highest at 72 h [(61.62 ± 26.55)% vs (10.17 ± 6.08)%; t = - 5.018, P = 0.015]. Determined at different time points byimmunohistochemistry and Western blotting assays, the AQP1 expression in mousehippocampus was constantly higher in TBI group than in sham group (P < 0.05), and reached the peak at 24 h (0.69 ± 0.32 vs 0.15 ± 0.07, t = - 4.335, P = 0.023 and 0.46 ± 0.19 vs 0.14 ± 0.04, t = -4.113, P = 0.004, respectively).  Conclusions Theup-regulation of AQP1 in mouse hippocampus after TBI perhaps participates inedema formation and delayed apoptosis of hippocampus, and AQP1 may be a newtherapeutic target to protect hippocampus from secondary injury after TBI.

 

doi: 10.3969/j.issn.1672-6731.2014.03.016

【 授权许可】

Unknown