煤工尘肺模型大鼠脑组织中ICAM-1及COX-2表达的研究

Study on expression of ICAM-1 and COX-2 in the brain tissue of CWP rats

目的:检测脑组织中细胞间黏附分子-1(ICAM-1)和环氧合酶-2(COX-2)的表达,探讨煤尘大鼠发生脑组织损伤的可能机制。方法:建立煤工尘肺大鼠模型并设立生理盐水对照组,同等条件下饲养16周后测血气分析并将其处死,采用免疫组化分析方法检测大鼠大脑皮质ICAM-1和COX-2的表达情况。同时,脑组织标本行尼氏染色,光镜下观察神经元细胞并计数。肺组织标本行HE染色,光镜下观察。结果:模型组ICAM-1和COX-2表达平均光密度值分别为(0.245 4±0.027 6)、(0.252 7±0.024 5),对照组分别为(0.154 1±0.010 5)、(0.153 9±0.032 8),尼氏染色平均神经元细胞数目模型组与对照组分别为(31.70±3.68)、(50.70±3.20)。两组比较,差异均有统计学意义(均P<0.01)。结论:ICAM-1及COX-2表达增加所产生的炎性作用可能是煤工尘肺大鼠并发脑组织损伤的重要机制之一。

Objective： To explore the possible mechanism of the coal-dust rats brain damage occurred by detecting the expression of brain cell ICAM-1 and COX-2.Methods： Coal worker pneumoconiosis model of rats and the salt water control were established,under the same conditions for 16 weeks after feeding measuring blood gas analysis and its execution,detecting the expression of ICAM-1 and COX-2 in cerebral cortex by the way of immunohistochemical method.Meanwhile,the brain tissue samples were Nissl stained neurons observed under light and counted.HE staining of lung tissue specimens were observed under light microscope.Results： In the model group,ICAM-1 and COX-2 expression in the average optical density values were（0.245 4±0.027 6）,（0.252 7±0.024 5）,the control group were（0.154 1±0.010 5）,（0.153 9±0.032 8）,Nissl average number of neurons model group and control group were（31.70±3.68）,（50.70±3.20）.There were significant differences in the two groups（all P0.01）.Conclusion： The increased expression of ICAM-1 and COX-2 produced by inflammatory effect may be one of the most important mechanisms about complicated by pneumoconiosis brain damage in rats.