Establishment of composite experimental animal model of brain edema after cerebral hemorrhagic.

Background: The aim of our study was to explore the establishment of an animal model of compound cerebral edema and assist the study of brain edema.

Methods: Sprague Dawley (SD) rats were randomly divided into 6 groups: Group A (IV collagenase + heparin autologous blood + non-heparin autologous blood), Group B (heparin autologous blood), Group C (IV collagenase), Group D (non-heparin autologous blood), Group E (control), Group F (sham); groups A, B, C, and D were modeled, group E received no treatment, and group F was injected with normal saline. The Longa/Bederson scales were used to test limb symmetry and score neurological deficits. The composition of brain tissue were measured by potassium (K+), sodium (Na+), and calcium (Ca2+). The glial cells were also subjected to primary culture and identification. The flow cytometry technique (FCM) and terminal uridine nick-end labeling (TUNEL) test were used to detect for the apoptosis of glial cells. Cell counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assays were used to observe the proliferation of glial cells; quantitative real-time polymerase chain reaction (qPCR) and western blot measured glial cell matrix metalloproteinase 9 (MMP-9) hole channel protein 4 messenger (m)RNA, and protein expression. The scratch and transwell tests were used to study the glial cell migration and invasion.

Results: Among all groups, according to the results of the Longa/Bederson scores of neurologic impairment, brain tissue water content, and electrolyte K+, Na+, Ca2+, group A showed the most significance (P<0.05). Group A showed the highest rate of apoptosis (32.27±3.33), least proliferation (5.33±1.14), and migration and invasion ability were the weakest (85.35±8.11; 8.08±1.96). The mRNA (9.31±0.84; 15.69±1.77) and protein (4.25±0.27; 4.34±0.33) of MMP-9 and aquaporin-4 (AQP4) were the most significant in group A (P<0.05). Inter-group comparison of groups B, C, and D and between groups E and F yielded no significant differences (P>0.05).

Conclusions: By using the obvious signs of brain edema, we were able to establish a composite experimental animal model for the study of brain edema after cerebral hemorrhage, to provide a reliable experimental basis for the study of brain edema.