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目的:探索慢性胃炎中无症CSG、无症CAG、有症F型、有症CSG和有症CAG的病理生理学渊由。 方法:对188例患者,应用透射电镜、能谱仪、图像分析仪与化学发光法等现代科学技术手段,同步检测胃黏膜上皮细胞超微结构、微量元素、DNA和SOD,以及LPO。 结果:胃黏膜上皮细胞核Zn、Cu、DNA和血清LPO含量,健康对照组(7.6±0.4,58.4±0.3,12.6±2.7,2.6±0.6),无症CSG组(7.8±0.3,58.6:0.4,13.0±3.1,2.9±0.4),无症CAG组(7.8±0.3,58.7±0.3,14.3±2.8,3.1±0.4),有症F型组(7.9±0.4,58.7±0.5,13.5±4.6,2.9±0.7),有症CSG组(8.1±0.5,58.9±0.5,15.2±3.2,4.2±0.7),有症CAG组(8.6±0.4,59.3±0.5,16.5±3.1,4.5±0.6);而线粒体Zn、Cu和胃黏膜SOD含量,健康对照组(9.2±0.5,58.3±0.3,170.5±6.1),无症CSG组(8.9±0.5,58.2±0.3,167.2±5.3),无症CAG组(8.8±0.4,57.5±0.2,166.1±4.2),有症F型组(8.9±0.5,58.0±0.3,167.9±5.7),有症CSG组(8.6±0.5,57.8±0.3,163.3±5.6),有症CAG组(8.3±0.4,57.5±0.3,161.2±4.3),组间均有显著性差异,P<0.05～0.001。胃黏膜上皮细胞超微结构与此发生同步变化。 结论:有病有症、有病无症、无病有症都发生在胃黏膜上皮细胞超微结构及其相关的生物活性物质的质量变化的基础上。
Objective: To explore the pathophysiology of chronic gastritis in asymptomatic CSG, asymptomatic CAG, symptomatic F-type, symptomatic CSG and symptomatic CAG. Methods: 188 patients were examined by electron microscopy, energy dispersive spectroscopy, image analyzer and chemiluminescence assay. The ultrastructure, trace elements, DNA and SOD, and LPO of gastric mucosal epithelial cells were simultaneously detected. Results: The contents of Zn, Cu, DNA and serum LPO in gastric mucosal epithelial cells were significantly higher in healthy control group (7.6 ± 0.4,58.4 ± 0.3,12.6 ± 2.7,2.6 ± 0.6) and asymptomatic CSG group (7.8 ± 0.3,58.6 ± 0.4, 13.0 ± 3.1,2.9 ± 0.4), SLE group (7.8 ± 0.3,58.7 ± 0.3,14.3 ± 2.8,3.1 ± 0.4), Symptomatic F group (7.9 ± 0.4,58.7 ± 0.5,13.5 ± 4.6,2.9 ± 0.7, 0.5 ± 0.5, 58.9 ± 0.5, 15.2 ± 3.2 and 4.2 ± 0.7 respectively) in the CSG group and 8.6 ± 0.4,59.3 ± 0.5,16.5 ± 3.1 and 4.5 ± 0.6 in the CAG group The contents of SOD, Zn, Cu and gastric mucosal SOD in healthy control group (9.2 ± 0.5,58.3 ± 0.3,170.5 ± 6.1), asymptomatic CSG group (8.9 ± 0.5,58.2 ± 0.3,167.2 ± 5.3) and asymptomatic CAG group ± 0.4, 57.5 ± 0.2, and 166.1 ± 4.2, respectively), F-type group (8.9 ± 0.5,58.0 ± 0.3,167.9 ± 5.7), CSG group (8.6 ± 0.5,57.8 ± 0.3,163.3 ± 5.6) Symptom CAG group (8.3 ± 0.4,57.5 ± 0.3,161.2 ± 4.3), there was a significant difference between groups, P <0.05 ~ 0.001. Gastric mucosal epithelial ultrastructure changes synchronously with this. CONCLUSIONS: Infectious disease, asymptomatic disease-free, disease-free and disease-free all occur on the basis of the change of the ultrastructure of gastric mucosal epithelial cells and the related mass of bioactive substances.