摘要
目的探讨应激性溃疡对大鼠胃黏膜损伤和对胃黏膜细胞连接相关蛋白VCL表达的影响及海马NMDA受体水平变化,为研究应激损伤的机制提供理论依据。方法运用小平台水环境法制造大鼠应激性溃疡模型,同时设立大平台组和正常对照组。实验共分为6组,每组5只,即正常对照组、大平台对照组、小平台应激1,3,5,7 d组。按照Guth标准计算胃黏膜损伤指数,采用免疫组化法分别同步观察应激性大鼠在不同时程胃黏膜的黏着斑蛋白和海马NMDAR2的变化,并对二者的相关关系予以分析。结果各应激组大鼠的溃疡指数均较正常对照组明显增加;随着应激时程的变化,胃黏膜VCL的表达呈现下降趋势;海马NMDAR2表达的水平在应激发生的初期开始降低,到造模的第3天,应激大鼠海马NMDAR2表达的水平已显著降低,到造模第5天,海马NMDAR2表达的水平开始上升。结论海马调控与应激性溃疡的发生密切相关,应激性溃疡发生时胃黏膜VCL表达下降。
Objective To investigate the expression of vinculin（VCL）in gastric mucosa and N-methyl-D-aspartate receptor 2 （NMDAR2）in hippocampus in rats of stress ulcer,and to provide a theoretical evidence for the mechanism of stress injury.Methods Stress ulcer model was induced in rats housed on the small platform over water.Controls were housed either in normal cages（CC）or on the large platform over water（TC）.The rats were randomly divided into six groups：CC group,TC group,stress 1 d group,3 d group, 5 d group and 7 d group.The ulcer index（UI）of gastric mucosa was quantified by Guth criterion.The expression of NMDAR2 in hippocampus and VCL in gastric mucosa in rats were detected by immunohistochemistry.Results UI was significantly higher in stress groups than in CC group.The expression of VCL in gastric mucosa was reduced in response to the stress in a time-dependent manner. The expression of NMDAR2 in hippocampus was decreased at the beginning of stress,and reached a minimum at 3 d.However,the expression of NMDAR2 in hippocampus increased gradually at 5 d.Conclusion These findings suggest that VCL is an important factor of the stress ulcer,and NMDAR2 also plays an important role in the regulation of stress ulcer.
出处
《山西医科大学学报》
CAS
2012年第10期727-730,803,804,共6页
Journal of Shanxi Medical University
