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Study on the pathophysiologic basis of classification of 'spleen' deficiency in chronic gastritis

机译:慢性胃炎“脾”虚证分类的病理生理基础研究

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Background Most of the studies on traditional Chinese medicine (TCM) 'spleen' deficiency syndrome in the recent 30 years were conducted only on the basis of single functional index, neglecting the study on the pathophysiologic internal relationship between spleen deficiency syndrome and gastric diseases in modern medicine. But it was at the subcellular molecular biological level that we explored the pathophysiologic basis of classification of spleen deficiency in chronic gastritis by detecting the bioactive substances in gastric mucosa nuclei and mitochondria. Methods By means of optical microscope, scanning electron microscope (SEM), transmission electron microscopy (TEM) and histochemical staining, we conducted histopathological, subcellular ultrastryctyral analysis and nuclei and mitochondrial ultrastructural analysis of gastric mucosa of 188 spleen deficiency patients and of 42 voluntary blood donors. At the same time, bioactive substances were measured by means of X-ray energy dispersive analysis system (EDAX) image analysis system, radioimmunoassay method and chemiluminescence method. Results The content of cAMP, superoxide dismutase (SOD), Zn and Cu in gastric mucosa, and the content of Zn and Cu in mitochondria decreased progressively in order of groups: healthy control (HC), spleen Qi deficiency without organic lesion (F-SQD), spleen Yang deficiency without organic lesion (F-SyangD), disease without symptoms group, spleen Qi deficiency with organic lesion (C-SQD), spleen Yang deficiency with organic lesion (G-SyangD), spleen Yin deficiency (SyinD) and spleen deficiency with Qi stagnation (SDQS), chronic spleen deficiency gastritis (CSG) and chronic atrophic gastritis (GAG); decreased in order of HC, intestinal metaplasia (IM) Ⅰ_a, IM Ⅰ_b, IM Ⅱ_a and IM Ⅱ_b, P < 0.05. The content of DNA, Zn and Cu in nuclei progressively increased in order mentioned above, P < 0.05. Conclusions The quantitative changes of gastric mucosal cAMP, SOD, Zn, Cu, of mitochondrial Zn, Cu and of nuclear DNA, Zn and Cu are not only the substance base on which the lesion of gastric mucosa tissue structure occurs, but also the substance base on which spleen deficiency is classified. G-SQD and G-SyangD were more likely to be found in low-grade or middle-grade CSG and CAG, while SyinD and SDQS in middle-grade or high-grade CSG, CAG and IM Ⅱ_b.
机译:背景技术近30年来,对中医“脾虚证”的研究大多仅基于单一功能指标进行,忽视了现代脾虚证与胃病的病理生理内在联系。药物。但是,在亚细胞分子生物学水平上,我们通过检测胃粘膜核和线粒体中的生物活性物质,探索了慢性胃炎脾脏不足分类的病理生理基础。方法采用光学显微镜,扫描电镜(SEM),透射电镜(TEM)和组织化学染色方法,对188例脾虚患者和42例自愿性血样患者的胃黏膜进行组织病理学,亚细胞超晶状体分析以及细胞核和线粒体超微结构分析。捐助者。同时,通过X射线能量色散分析系统(EDAX)图像分析系统,放射免疫分析法和化学发光法对生物活性物质进行了测定。结果胃粘膜中cAMP,超氧化物歧化酶(SOD),锌和铜的含量以及线粒体中锌和铜的含量依次降低:健康对照组(HC),无有机病变的脾气虚(F- SQD),无器质性病变的脾阳虚(F-SyangD),无症状组的疾病,有器质性病变的脾气虚(C-SQD),有器质性病变的脾阳虚(G-SyangD),脾阴虚(SyinD)脾气虚停(SDQS),慢性脾虚胃炎(CSG)和慢性萎缩性胃炎(GAG); HC,肠上皮化生(IM)Ⅰ_a,IMⅠ_b,IMⅡ_a和IMⅡ_b依次降低,P <0.05。核中DNA,Zn和Cu的含量按上述顺序逐渐增加,P <0.05。结论胃黏膜cAMP,SOD,Zn,Cu,线粒体Zn,Cu以及核DNA,Zn和Cu的定量变化不仅是发生胃黏膜组织结构病变的物质基础,而且是物质基础。脾虚的分类。低级或中级CSG和CAG中更可能出现G-SQD和G-SyangD,而中级或高级CSG,CAG和IMⅡ_b中更容易出现SyinD和SDQS。

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