| BackgroundRecent years, with the sharp increase in coal demand, coal production and the strength of increasing mechanization, production sites dust concentration rise, in some of China's coal-rich province, the high incidence of coal workers pneumoconiosis. CWP progress in the process of leaving easily combined with several complications, disease progression and even death. The survey found that since 2000, coal worker's pneumoconiosis complicated by cardiovascular and cerebrovascular brain disease in patients with CWP was promoted to major causes of death [1]. Therefore,to observe the mechanism of CWP merged with brain damage is significant for improving the quality of life of patients with pneumoconiosis and reducing mortality. Currently, studies reported on mechanism of brain tissue damage is less.Chronic hypoxia on brain damage is increasingly cause for concern. Studies suggest that cerebral hypoxia or ischemia can produce large amounts of inflammatory mediators [2-5]. Brain inflammation in the brain cortex damage pathogenic process plays a very important role. In this study, pneumoconiosis model through the establishment of this experiment to study the model due to the influence of brain tissue hypoxia and the resulting brain injury in ICAM-1 and COX-2 expression in both inflammatory cytokine and its significance.ObjectiveThrough the establishment of this experiment pneumoconiosis model , to observe the expression of intercellular adhesion molecule -1 (ICAM-1) and cyclooxygenase -2 (COX-2) in CWP rats brain cortex damage, preliminary study possible mechanisms of brain cortex damage, and the potential pathological significance.Methods(1) non-exposed intratracheally Preparation of experimental rat model of pneumoconiosis, (190±20) g male Wistar rats ,60 .All of the rats were randomly divided into three groups ,model group (30 rats) and the control group (30 rats). At the time points that treated for 4,8,20 weeks, 10 rats were selected in each group, adopt arterial 0.3 ml send blood gas analysis, immediately take brain bufo, free double lung and fixed specimens for paraffin embedding; (2) HE staining to observe dye dust morphological changes in lung tissue; (3) Nissle staining evaluation of rat brain cortex morphology; (4) Immunohistochemical analysis was used to detect ICAM-1 in cerebral cortex and the expression of COX-2, and from the expression and localization phase to evaluate the pathological significance of trends, exploring the mechanism of ICAM-1 and COX-2 in brain cortex damage; (5) All the data of experiment were analyzed by statistics software SPSS17.0.Results(1) Blood gas analysis results: Blood gas analysis for 4 weeks, 8 weeks, 20 weeks, model group, the average blood oxygen pressure was (85.51±7.09),(76.44±5.50),(69.79±6.91);The control group at each time point the average blood oxygen pressure was (97.85±4.91),(98.05±4.58),(96.41±5.25)。(2) pulmonary pathological observation: The first 4-8 weeks after dust, the pathological bronchial alveolar wall and has extensive inflammatory cell infiltration, mainly macrophages and lymphocytes, some alveolar swallowed a lot of dust visible in alveolar macrophages and the formation of coal dust gathering spots or nodules around the part of the increase in alveolar gas to expand. The first 20 weeks, we can see the lung tissue in model group with much collagen fiber hyperplasia lesions, large areas of pulmonary fibrosis.(3) Nissle staining: Model group at 8 weeks nuclear pyknosis Nissl bodies were reduced,the outline blurred, part of the cytoplasmic autolysis, uneven coloring, 20 weeks, reduce the number of neurons, nuclear pyknosis Nissl bodies were significantly reduced,particles drop out, the cytoplasmic autolysis; Control group, the number of neurons in brain tissue more closely and evenly, round or oval nuclei, prominent nucleoli, clear cytoplasm, and its rich in Nissl bodies evenly.(4) Immunohistochemical half quantitative results :①Brain cortex ICAM-1 mean optical density of 4 weeks, 8 weeks, 20 weeks in model group and control group were (0.2034±0.0075)(0.0378±0.0077),(0.2241±0.0076)(0.0286±0.0050),(0.2454±0.0276)(0.0348±0.0077);②COX-2 in brain cortex mean optical density of 4 weeks, 8 weeks, 20 weeks, the model group and control group were(0.2298±0.0121)(0.0585±0.0071),(0.2614±0.0188)(0.0550±0.0125),(0.2994±0.0119)(0.0530±0.1039).Conclusion1. Chronic hypoxia caused by Coal worker's pneumoconiosis may make rats cerebral cortex damage 2. ICAM-1, COX-2 expression increased generated by chronic hypoxia may be one of the more important mechanism during the process of coal worker pneumoconiosis complicated with cerebral cortex damage.
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