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

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.

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.

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).

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.