| ObjectivesTraumatic brain injury (TBI) is very common in neurosurgery. Many experimental and clinical researches have conformed that the secondary brain injury is an important pathological process after TBI. Recently, the results of oversea and domestic researches have indicated that inflammation after TBI play a critical role in the secondary brain injury. Inflammation contributes closely to brain tissue degeneration and necrosis, blood brain barrier (BBB) damage and local brain tissue edema after TBI. Leukocyte infiltration is a main characteristic of inflammation. Intercellular adhesion molecule-1 (1CAM-1) andmonocyte chemoattractant protein- 1 (MCP-1) are the key factors which activate and direct leukocytes moving out of capillary vessels and gathering in the inflammatory area. Therefore, ICAM-1 and MCP-1 are closely related to the inflammatory course after TBI.Many researches indicate that hyperbaric oxygen(HBO) treatment can effectively alleviate TBI in recovering consciousness, improving nervous function and improving prognosis. But the accurate mechanisms are not known. In the course of experimental study on re-perfusion of ischemic skeletal-muscle graft, Zamboni found that HBO could reduce leukocyte adhering to endothelia and infiltrating. Whether HBO affects leukocyte infiltration and the expression of ICAM-1 and MCP-1 in brain tissue has been not reported. The objectives of present experimental research are to explore the HBO influence on the expression of ICAM-1 and MCP-1 after TBI, which may provide the theoretical evidences for the effect of HBO in treating TBI.MethodsAdult healthy male SD rats are chosen. The range of their-5-weight was 250 - 300g. All rats were divided into two groups: group A and group B, then each group was divided into 6 sub-group at random. According to Freeney's experimental TBI model, moderate damage was done on all rats. No administration was done on group A and group B were sent to HBO treatment in 30 minutes after TBI. Then the rats of sub-group 1,2,3,4,5,6 were killed at 3h, 6h, 12h, 24h, 72h and on day 7 respectively after TBI. One part of each specimen was sent to electron microscope center, the rest was stained with immunohistochemical method of ICAM-1 and MCP-1. The positive cells were measured by map analysis system(MAS). The results were analysized by SPSS on computer. Data were expressed as x s with a =0.05 considered statistically significant.Results1, The change of brain tissue ultrastructure under electromicroscopeIn group A, vascular periphery edema and mitochondria swollen were obviously observed at 3h after TBI. At 6h, vascular periphery edema was the most apparent and mitochondria was ball-like, even blebbing and fragmentary. Mitochondria matrixes vanished. At 12h, the conditions were alleviated. Vascular periphery edema in every sub-group ofgroup B was slighter than that of group A respectively. The blibbing and fragmentary of mitochondria wasn't exist in group B. At 24h, both group A and B showed no significant difference .2, The expression of ICAM-1In group A, the expression of ICAM-1 began to up-regulate at 3h and the expression reached the highest level at 6h and began to reduce after 24h. The expression of ICAM-1 became minor on 7th day after TBI. The expression of ICAM-1 in group B was dramatically lower than that in group A at 3h, 6h and 12h respectively (P<0.05). However, the conditions in both group A and B had not difference at 24h after TBI ( P>0.05 ) . 3, The expression of MCP-1In both group A and B, the expression of MCP-1 began to be observed at 3h after TBI, and the expression reached the highest level at 12h, and the expression was high at 24h after TBI. But, the expression of MCP-1 in each sub-group of group B was lower than of group A at 3h, 6h, 12h and 24h respectively after TBI (P<0.05). The expression of MCP-1 in both group A and B showed no significant difference (P>0.05) . The expression of MCP-1 was faint on 7 day after TBI.-7-Conclusion1, A critical characteris...
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