| Intracerebral hemorrhage (ICH) is associated with high mortality and Morbidity. In addition to the mass effect and direct disruption, the secondary injury is also the main cause after ICH. An average-sized hematoma in humans (54ml) has little immediate effect on intracranial pressure or cerebral perfusion pressure because that volume is well with the volume-buffering capacity of the intracranial space. There is evidence that intracerebral blood causes brain injury through biochemical substances released from the hematoma that initiate formation of brain edema. Thrombin, released from the coagulation cascade after experimental ICH, leads to edema formation and disruption of blood-brain-barrier. The important role of thrombin after ICH is already affirmed, but its accurate mechanism is still unclear. The structure of the cytoplasm relies on the assembly and organization of a network of fibrous components, which includes microtubules, microfilaments, and intermediate filaments. The cytoskeleton is implicated in a wide variety of functions that are essential for cellular life including mitosis, maintenance of cell shape, motility, intracellular transport of organelles, and secretary processes. Microtubules have been isolated mainly from brain, where tubulin, a major microtubular component, is present in significantly larger amounts than in other tissues. Even though tubulin can self-assemble in vitro into microtubules under appropriate conditions, the presence of MAPs is required for in vivo assembly of tubulin. MAPs promote the assembly of tubulin and suppress its disassembly. MAP-2 is present in larger amounts in brain than in other tissues. Microtubule-associated protein-2 is found mainly in dendrites and soma of neural cells in most regions of the central nervous system. The high levels of expression of these MAP-2 in neurons, their selective associations to either axonal or dendritic compartments, and their developmental regulation support a putative role of MAP-2 as mediators of neuronal morphogenesis. Glial fibrillary acidic protein is a marker for astrocyte as well as one of the cytoskeleton components. There are densely distributed GFAP-positive cells around the blood clot, and the number and morphological features of GFAP-positive astrocytes changed as time went on after ICH. One hand, the activated astrocytes have protective functions, such as promoting the formation of glial scar to escape from reblooding; secreting various neural protective factors to accelerate the repairation of the injury. On the other hand, excessive glial reaction will affect the restoration of peripheral tissue structure and function because impair the regeneration of myelinated and axon; moreover, they will release glutamic acid and nitrous oxide which can destroy the nervous system; the glial reaction also produce inflammation medium, such as IL-1β and TNF-α resulting in the opening of the blood brain barrier, mediating inflammation reaction, accelerating the necrosis of endothelium to participate in the pathology of brain edema. Objective: To explore the role of thrombin in the pathological mechanism of ICH by observing the expression of MAP-2 and GFAP in the perihematomal brain regions, and the protective mechanism of hirudin. Methods: The rat was positioned in a stereotactic frame, rat models of ICH were made by infusion of autologous blood into the right neucleus caudatus (coordinates: 0.2mm anterior, 5.5mm ventral, and 4mm lateral to the bregma). Large Wistar rats were divided randomly into three groups. Group 1: normal control group. Group 2 : pure intracerebral hemorrhage group, the animals were sacrificed respectively on the 6h , 1d, 2d, 3d, and 7d after blood infusion. Group 3: hirudin group (the administration of hirudin after blood infusion), the animals were sacrificed respectively on the 3d, and 7d after the administration of hirudin. Each group and each time phase included 5 rats respectively. Brains were examined by water content and conventional histologic and immunohistologic...
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