Experimental Research: Experssional Changes Of Glucocorticoid Receptor Following Local Traumatic Bain Injury Of Mouse

Objective: Using the local traumatic brain injury(TBI) model of mouse as a research platform to investigate the expressional changes of Glucocorticoid Receptor(GR) and its mRNA following traumatic brain injury in order to study the time characteristics of GR expression after traumatic brain injury. To preliminarily investigate the expressional feature and regulative site of GR in different molecular levels and to provide exprimental bases for exploring the biological effects of GR in TBI and to assess the rationality of glucocorticoid therapy in clinical works.Methods: Based upon the Feeney′S model ,a total of 42 SD rats, weighting around 300g,were used in this study. They were randomly divided into control group(n=6) and injury group(n=36),and then the later was subdivided into 1hour﹑6﹑12﹑24﹑48 and 72hours six different points after brain injury, every point had 6 rats(Immunohischemistry n=3 and RT-PCR n=3). Immunohi -schemistry and RT-PCR were respectively used to analyze GR and its mRNA expressions and subcellular localization at different time points in early stage after traumatic brain injury.Results: In the normal brain tissue, a widespread distribution of GR had been demonstrated in the cytoplasm and nucleus of neurons and glial cells, but no changes were found in membrane. The expression of the GR in brain tissue significantly decreased from 1 hour after traumatic brain injury and reached the lowest at 24 hours (compared with control group ,P <0.05) ,then gradually recovered ,reached 82.76% compared with normal at 72 hours;mRNA of Glucocorticoid Receptor gradually decreased from 1 hour after traunmatic brain injury , reached the lowest at 12 hours(compared with control group ,P <0.05) ,recovered to 79% compared with normal control at 72 hours.Conclusion: GR and mRNA were lowly expressed in early time after traumatic brain injury ,the regulative site may be at the transcriptional level and redistribution of GR in the cell caused by nuclear translocation possibly involves in the functional regulation of GR.,but the investigation of detailed regulatory mechanisms needs ongoing studies. The functional decreasing of GR may be related with this.So the rationality of glucocorticoid therapy in clinical works need to consider the effect of GR expression level and its funtional status in brain tissue after brain injury .