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目的研究缺血性脑卒中时是否存在肠黏膜屏障改变以及紧密连接蛋白Zonula Occluden-1(ZO-1)在其中的可能机制。方法杂犬20只,随机分为实验组和对照组,每组10只。实验组用双硅柱法制作缺血性脑卒中模型。实验前、实验后0.5、3、6、12、24h行血浆二胺氧化酶(DAO)活性和D-乳酸(D-lac)浓度检测;光镜下对肠黏膜病理形态进行观察;免疫组化法分析肠黏膜ZO-1蛋白的表达。结果和对照组比较,实验组24hDAO、12h和24hD-lac明显增高(24h DAO:0.5512±0.1057比0.3822±0.0789;12hD-lac:6.2249±1.2683比4.3342±0.7900;24hD-lac:8.4581±1.7416比4.4766±0.9486;P<0.01);实验组ZO-1蛋白平均光密度(OD)明显降低(0.1989±0.0118比0.2224±0.0150;P<0.01)。相关和回归分析显示,血浆24hDAO与24h、12h、6hD-lac呈正相关关系(γ分别为0.787、0.8117、0.862,P<0.01);ZO-1蛋白OD与24hDAO、24hD-Lac呈负相关(γ分别为-0.8385、-0.7088,P=0.002、0.022),光镜下观察,实验组存在小肠病理损伤,对照组小肠结构正常。结论血浆DAO活性和D-lac能有效反映缺血性脑卒中时肠屏障损伤。肠黏膜紧密连接蛋白ZO-1在缺血性脑卒中时表达降低,这是肠屏障功能障碍的重要分子机制之一。
Objective To investigate whether there is a change of intestinal mucosal barrier in ischemic stroke and the possible mechanism of the tight junction protein Zonula Occluden-1 (ZO-1) in it. Methods Twenty dogs were randomly divided into experimental group and control group with 10 rats in each group. Experimental group using double silica column method of making ischemic stroke model. The plasma DAE activity and D-lactate (D-lac) concentration were measured at 0.5, 3, 6, 12 and 24 hours after the experiment. Pathological changes of intestinal mucosa were observed under light microscope. Method analysis of intestinal mucosa ZO-1 protein expression. Results Compared with the control group, the 24hDAO, 12h and 24hD-lac in the experimental group were significantly increased (24h DAO: 0.5512 ± 0.1057 vs 0.3822 ± 0.0789; 12hD-lac: 6.2249 ± 1.2683 vs 4.3342 ± 0.7900; 24hD-lac: 8.4581 ± 1.7416 vs 4.4766 ± 0.9486; P <0.01). The average optical density (OD) of ZO-1 protein in the experimental group was significantly decreased (0.1989 ± 0.0118 vs 0.2224 ± 0.0150; P <0.01). Correlation and regression analysis showed that there was a positive correlation between plasma 24hDAO and 24h, 12h and 6hD-lac (γ = 0.787,0.8117,0.862, P <0.01). The OD value of ZO-1 was negatively correlated with 24hDAO and 24hD-Lac Respectively, -0.8385, -0.7088, P = 0.002,0.022). Under light microscope, there was intestinal pathological damage in the experimental group and normal intestinal tissue in the control group. Conclusions Plasma DAO activity and D-lac can effectively reflect intestinal barrier injury in ischemic stroke. Intestinal mucosal tight junction protein ZO-1 in ischemic stroke decreased expression, which is one of the important molecular mechanisms of intestinal barrier dysfunction.