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目的研究慢传输型便秘结肠肌间神经丛的神经丝蛋白和 S-100蛋白的病理改变,探索结肠动力减弱的原因,为临床治疗提供理论依据.方法采用免疫组织化学方法研究33例结肠慢传输型便秘患者(STC 组)和25例非便秘性结肠(对照组)的升结肠、横结肠、降结肠、乙状结肠的肌间神经丛内神经丝蛋白和 S-100蛋白的表达,利用计算机图象分析系统作定量分析,并与病程及年龄作直线相关性分析.所得数据用 t 检验进行统计学处理.结果对照组结肠肌间神经丛内神经丝蛋白和 S-100蛋白的含量在各段之间无显著性差别(0.09±0.03 vs 0.10±0.02,P>0.05),STC 组结肠各段与对照组比较,神经丝蛋白的平均光密度值明显高于对照组(0.12±0.03 vs 0.09±0.02,P<0.01);S-100蛋白的含量及平均光密度值明显高于对照组(0.10±0.04 vs 0.08±0.03,P<0.01).神经丝蛋白和 S-100蛋白的改变随着病程的延长而增加,二者呈直线相关(r=0.75)结论慢传输型便秘结肠肌间神经丛存在着全结肠性退行性病理改变,表现为神经丝蛋白的堆积聚集和神经间质的增生,且随着病程的延长而加重,这是造成结肠动力减弱的主要原因.提示,手术切除结肠的范围应是全结肠或次全结肠.
Objective To study the pathological changes of neurofilament protein and S-100 protein in the slow-transit constipation colon myenteric plexus and to explore the reasons for the weakening of colonic motility and to provide a theoretical basis for clinical treatment.Methods 33 cases of slow transit of colon were studied by immunohistochemistry Type constipation patients (STC group) and 25 cases of non-constipation colon (control group) in the ascending colon, transverse colon, descending colon and sigmoid myenteric plexus neurofilament protein and S-100 protein expression using computer image analysis The system for quantitative analysis, and with the course and age for linear correlation analysis.The data were statistically analyzed using t test.Results The control group colon myenteric plexus neurofilament protein and S-100 protein content between the segments There was no significant difference (0.09 ± 0.03 vs 0.10 ± 0.02, P> 0.05). Compared with the control group, the average optical density of neurofilament in STC group was significantly higher than that in control group (0.12 ± 0.03 vs 0.09 ± 0.02, P <0.01). The content and average optical density of S-100 protein were significantly higher than those of the control group (0.10 ± 0.04 vs 0.08 ± 0.03, P <0.01) And increase, the two were straight Conclusion (r = 0.75) Conclusion slow transit constipation colon myenteric plexus there is a full colon degenerative pathological changes, manifested as neurofilament accumulation and accumulation of neuronal interstitial hyperplasia, and as the duration of the disease aggravated, This is the main cause of impaired colon motility, suggesting that the scope of resection of the colon should be the whole colon or subtotal colon.