| Intracerebral hemorrhage (ICH) means non - traumatic parenchymal hemorrhage and is associated with extremely high rates of mortality and morbidity. Currently, no definite treatment is available for ICH. A poor understanding of the pathophysiological process underlying neuronal injury after ICH is responsible for the lack of effective therapies. Proinflammatory cytokine synthesis and release occurs early in the development of focal cerebral ischemia and traumatic head injury. The production of cytokines and chemokine messenger ribonucleic acid coincident with or preceding the infiltration of polymorphonuclear leukocytes invasion in experimental central nervous system injury has suggested a role in the pathophysiology of neural injury. As the pathogenesis of ICH were studied profoundly , most scholar found that immunologic reaction directly took part in most pathophysiological process after ICH.Proinflammatory cytokine was little molecular polypeptide with extensive immunoactive, was synthesized by immunocyte, monocyte, lymphocyte, fibro-blast and endothelial cell and took part in most immunologic reaction. To our knowledge, central nervous svstem possessed the same immunological response process as external immune system. With gene expression analysis, we found that neuron itself could synthesize a lot of proinflammatory cytokines and their receptors, simultaneously express many receptors of proinflammatory cytokines. Conditions such as brain injury, inflammation and infection could cause extensive immunocyte to enter brain or activate neuroglial cell and neuron to excrete proinflammatory cytokines that took part in formation and developmentof brain e-dema as well as damage plerosis and regeneration of neuron. At present, studies has been showed neuroglial cell and neuron could excrete IL -1 IL -2 IL -3 IL -4 IL -6 TNF - Aand TGF so on, whose action was temporary and regional. Proinflammatory cytokines played an important role in regulation and instruction.IL -2 and IL - 8 were two of the main proinflammatory cytokines that introduced inflammation. Recently, most of the domestic and abroad studies on IL -2 IL -8 in cerebrovascular disease lay in their changes and application in cerebral infarction, whereas little in ICH. In our experiment, the animals were injected fresh autologous artery blood into the caudate nucleus by an oriented can-nula. The contents of IL - 2 and IL - 8 in brain tissues at each time point were determined with Rl(radioimmunoassay) ; the cerebral water content was measured with wet - dry weight method. The aim was to investigate the expression of IL -2 IL -8 and their significance.Materials and Methods1. Preparation of experimental animals: fifty - two healthy male Wistar rats who were randomly divided into the control group ( n = 12 ) and the treatment group (n =40), weighing 300 -340g, were studied. The control group included the one - day group (n = 6) and three - day group ( n = 6 ) , whereas the treatment group included six - hour group one - day group three - day group six - day group and ten -day group; each group had eight rats.2. Preparation of animal models: the animals were anesthetized with Chloral Hydrate (350mg/kg) administered Intraabdominally and placed in a rat ster-eotactic frame (Jiang Wan I type). The rat's head was fixed in a head frame, and a hole was drilled 2 mm anterior to the bregma and 3 mm lateral to the mid-line on the right side. Autologous nonheparinized arterial blood (200ul) was loaded into a 1 ml - injector. To induce hematoma in the treatment group, the 1ml - injector was introduced to a depth of 6mm below the surface of the skull, subsequently 100 ul autologous blood was slowly infused into each of thirty animals ; a second group of twelve animals (control group) underwent intracranial needle placement without blood injection. The injection time ranged from twenty-five to thirty minutes. Rectal temperature was monitored and maintained between 36℃. and 37℃ through the experiment. After injection, the needle was removed, the...
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