Vascular Endothelial Growth Factor And Glial Fibrillary Acidic Protein Expression Changes In Experimental Intracerebral Hemorrhage In The Rat Brain

Objectives: Intracerebral hemorrhage (ICH) is one of the most common clinical diseases. More attention is payed to how to reduce the disability and mortality after ICH. Pathological and experimental studies have indicated that the reduction of local cerebral blood flow and progressive ischemic damage of tissue occurred in regions surrounding a hematoma after ICH. The secondary brain injury is key for prognosis after ICH. Vascular endothelial growth factor (VEGF) is a specific regulator that can promote the proliferation of endothelial cell and enhance the vascular permeability. Astrocytes can response sensitively to the brain injury, which can be testified by glial fibrillary acidic protein (GFAP). The latter one is also an important marker since it can reflect the bioactivity of the astrocytes. The objectives of the studies were to observe the expression of VEGF.. FVIH-R Ag and GFAP in rats brain tissue in the border zone of the hematoma, and explore the relationship between the expression of VEGF and the brain edema as well as the brain angiogenesis after ICH. Methods: In 60 adult SD rats, intracerebral hemorrhage was induced by injection of 0.5u (0.5 p. 1) Type VII collagenase into the right caudate nucleus. The rats were randomly divided into two groups, control and experimental ICII groups. The morphological studies were performed in serial sections at 12h, ld, 3d and 7d after ICH, respectively. Brain water content was calculated by using dry-wet weight method. The immunohistochemical method and computer image analysis were performed in rats brain by using different anti- sera of VEGF~ FVBI-R Ag and GFAP. Pathological changes in the same area were observed with transmission electron microscope. Results: (1). Compared with the controls, brain water content in the experimental group was significantly increased in the ipsilateral brain at 1 2h after ICI-I (p<0.05). At ld, brain water content was reached its peak and returned toward normal level at 7d gradually. (2). Neuron edema, degeneration and necrosis were observed in ultrastructure at different time points, endothelial cells edema were also discovered. (3). The amount of VEGF positive cells was markedly increased, and reached the highest at 7d in the border zone after ICH (p<0.0 1), but there were no significant difference among the mean value of OD of cells at different time points (p>0.05). (4). Cell-counting study showed that the FVBI-R Ag positive endothelial cells and GFAP inimunostained astrocytes were markedly increased and a peak was noted at 7d after ICH. The OD of cells was significant difference at different time. Conclusions: The results of these experimental studies suggested that the border zone of ICH consisted of zone of compression and zone of edema. The upregulated expression of VEGF might induce proliferation of endothelial cell and angiogenesis in the border zone after ICH in rats; there might be no relationship between expression of VEGF and brain edema formation in early period of ICH. GFAP-reactive astrocyte hypertrophy and hyperplasia and angiogenesis might play an important role in ischemic neurons recovery and damaged tissue repair after ICH. Therefore, it is possible to reduce the brain injury after ICH through use of VEGF as a treatment strategy.