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

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 ultrastructural 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 (G-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 (CAG); decreased in order of HC, intestinal metaplasia (IM)Ia, IMIb, IMIIa and IMIIb, 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 IMIIb.

Effect of Weikangfu granule on the physiopathologic figure of precancerosis of gastric mucosa in patients of chronic gastritis with Pi-deficiency syndrome.

OBJECTIVE: To study the physiopathologic basis of Weikangfu Granule (WKFG) in treating precancerosis of gastric mucosa in patients of chronic gastritis with Pi-deficiency syndrome (CG-PDS). METHODS: One hundred and fifteen patients of CG-PDS who suffered from intestinal metaplasia (IM) and atypical hyperplasia (ATHP) of gastric mucosa, were divided into two groups. The treated group (n = 61) was treated by WKFG with its ingredients modified according to the syndrome type of patients. The control group (n = 54) was treated with Weishu granule. The histopathological and subcellular ultrastructural changes were detected by optical microscope, screening electronic microscope, transmission electronic microscope and histochemical staining; the nuclear and mitochondrial ultrastructure of gastric mucosa were analyzed with energy dispersion X-ray analyser and image analysis system. And the changes of cAMP, lipid peroxide (LPO), superoxide dismutase (SOD) before and after treatment in the treated group were measured and compared with those of the health control group consisting of 15 volunteers. RESULTS: The symptomatic and pathological therapeutic effect in the treated group were significantly superior to those in the control group (P < 0.05). The contents of Zn, Cu, cAMP, SOD and (3)H-TdR LCT in gastric mucosa of the treated group before treatment were all lower than those of the healthy control group, yet all these indexes markedly increased after treatment, while serum LPO level, which increased before treatment was lowered after treatment. All the changes showed statistical significance (P < 0.05 or P < 0.01). CONCLUSION: WKFG can reverse IM and ATHP in patients of CG-PDS, and the effect may be realized by way of increasing the level of Zn, Cu, cAMP and SOD in gastric mucosa, promoting cell differentiation, enhancing cellular immunity and reducing oxygen free radicals and lipid peroxidation.

Study on the pathological basis of classification of spleen deficiency in chronic gastritis.

BACKGROUND: Spleen in Traditional Chinese Medicine (TCM) is not actually the spleen in the anatomic sense designated in western medicine because its functions basically belong to the physiological category of digestive system in modern medicine, and it represents a macroscopic concept of digestion, absorption and nutrition metabolism. Spleen deficiency syndrome refers to the clinical phenomena such as hypofunction of digestion, absorption and nutrition metabolism. By integrating TCM with modern medicine, this paper is intended to explore the pathological basis of classification of spleen deficiency in chronic gastritis. METHOD: By means of optical microscope, scanning electron microscope (SEM), transmission electron microscope (TEM) and histochemical staining, we conducted histopathological and subcellular ultrastructural (nuclei and mitochondrial) analysis of gastric mucosa of 188 patients of spleen deficiency, and that of 42 voluntary blood donors without clinical symptoms. RESULTS: The gastric mucosa of patients with spleen Qi deficiency (SQD) and spleen yang deficiency (SyangD) could either be affected by organic lesion (type G-occurring on the basis of chronic superficial gastritis (CSG), chronic atrophic gastritis (CAG)) or unaffected (type F-chiefly belonging to functional indigestion); spleen yin deficiency (SyinD) and spleen deficiency with Qi stagnation (SDQS) both occurred on the basis of CSG and CAG; and the degree of mucosa inflammatory cells infiltration, the degree of decrease in glands propria, and the incidence of IMIIb in CSG and CAG were more serious than those of G-SQD and G-SyangD, P < 0.05 - 0.01. CONCLUSION: Spleen deficiency syndrome is likely to occur on the basis of organic lesion of gastric mucosa (disease with symptoms of both CSG or CAG and spleen deficiency symptoms), as well as on the basis of inorganic lesion of gastric mucosa (nondisease with symptoms, which is, despite spleen deficiency symptoms, there is no CSG or CAG). Besides, the clinical phenomenon of disease without symptoms (despite CSG or CAG, there is no spleen deficiency symptoms) occurres because of such factors as genetic diathesis and compensation. The lesion degree of CSG or CAG and the incidence of IMIIb of SyinD and SDQS are more serious than those CSG and CAG of G-SQD and G-SyangD.

Study on the classification of chronic gastritis at molecular biological level.

AIM: To explore the pathophysiologibasis for the fact that patients with digestive tract symptoms do not necessarily have gastric mucosal pathology and those without clinical symptoms do not necessarily have no gastric mucosal pathology. METHODS: The ultrastructure, trace elements, cAMP, DNA, SOD and LPO in the gastric mucosa and its epithelial cells of 188 patients without organic lesions of heart, lung, liver, gallbladder, pancreas, kidney or intestine and basically histopathological normal persons (F) were detected synchronously by SEM, TEM, EDAX, Image analysis system RIA and (3)H-TdR Lymphocyte Transfer Test. RESULTS: The content of Zn, Cu, cAMP and (3)H-TdR LCT in gastric mucosa and the content of Zn, Cu, DNA and LPO in gastric mucosa epithelial nuclei of each group were shown as belows: Normal control (4.1+/-1.0, 5.2+/-0.8, 15.9+/-1.5, 1079.7+/-227.4, 7.6+/-0.4, 58.4+/-0.3, 12.6+/-2.7, 2.6+/-0.6); CSG without symptoms group (3.7+/-1.2, 5.1+/-1.8, 15.6+/-0.9, 924.5+/-234.9, 7.8+/-0.3, 58.6+/-0.4, 13.0+/-3.1, 2.9+/-0.4); CAG without symptoms group (3.3+/-1.0, 4.8+/-0.9, 14.9+/-0.7, 887.7+/-243.6, 7.8+/-0.3, 58.7+/-0.3, 14.3+/-2.8, 3.1+/-0.4); F type with symptoms group (3.5+/-1.4, 4.5+/-1.0, 15.7+/-1.4, 932.1+/-2449.3, 7.9+/-0.4, 58.7+/-0.5, 13.5+/-4.6, 2.9+/-0.7); CSG with symptoms group (2.8+/-1.9, 4.0+/-1.5, 14.2+/-1.8, 867.3+/-240.5, 8.1+/-0.5, 58.9+/-0.5, 15.2+/-3.2, 4.2+/-0.7); CAG with symptoms group (2.0+/-1.8, 3.4+/-1.5, 13.4+/-1.8, 800.9+/-221.8, 8.6+/-0.4, 59.3+/-0.5, 16.5+/-3.1, 4.5+/-0.6). The contents of Zn, Cu in mitochonondria and SOD in gastric mucosa of each group were shown as belows: Normal control group (9.2+/-0.5, 58.3+/-0.3, 170.5+/-6.1), CSG without symptoms group (8.9+/-0.5, 58.2+/-0.3, 167.2+/-5.3), CAG without symptoms group (8.8+/-0.4, 57.5+/-0.2, 166.1+/-4.2); F type with symptoms group (8.9+/-0.5, 58.0+/-0.3, 167.9+/-5.7), CSG with symptoms group (8.6+/-0.5, 57.8+/-0.3, 163.3+/-5.6); CAG with symptoms group (8.3+/-0.4, 57.5+/-0.3, 161.2+/-4.3). There were significant differences in these cases, P<0.05-0.001. There were synchronous changes of gastric mucosa epithelial cellular ultrastructure. The "background lesions" (focal atrophic gastritis, focal intestinal metaplasia, micro-ulcer) in nonfocal gastric mucosa of all groups had significant differences (P<0.05-0.001). CONCLUSION: Disease with symptoms, disease without symptoms, nondisease with symptoms occur on the basis of the quantitative changes of gastric mucosa epithelial cellular ultrastructure and related bioactive substances.

Ultrastructure and molecular biological changes of chronic gastritis, gastric cancer and gastric precancerous lesions: a comparative study.

AIM: To carry out a comparative study on ultrastructure and molecular biological changes of chronic gastritis (CG), gastric cancer (GC) aand gastric precancerous lesions. METHODS: By the use of histochemical staining, SEM with EDAX, TEM with EDAX, image analysis technique, RIA and chemiluminescence method, gastric mucosa of 168 patients were synchronously analyzed in morphology, trace elements, DNA, cAMP, SOD, (3)H-TdR LCT and serum LPO were also done. RESULTS: The incidence of epithelial nucleoplasmic ratio >1, lobulated nuclei, inter-chromatin aggregation of granules, nucleolar hypertrophy, and the content of DNA, Zn, Cu in nuclei and serum LPO of each group were showed as belows: normal control group (0.0, 0.0, 6.7, 0.0, 12.6+/-2.7, 7.6+/-0.4, 58.4+/-0.3, 2.6+/-0.6), CSG group (5.7, 2.9, 7.4, 2.9, 15.2+/-3.1, 8.1+/-0.5, 58.9+/-0.5, 4.2+/-0.7), CAG group (31.3, 29.7, 45.3, 42.2, 16.5+/-3.1, 8.6+/-0.4, 59.3+/-0.5, 4.5+/-0.6), CA group (100.0, 100.0, 72.2, 50.0, 30.7+/-8.2, 8.8+/-0.3, 59.5+/-0.4, 6.8+/-1.6), ATP(++) group (61.5, 38.5, 23.1, 38.5, 23.5+/-8.9, 8.3+/-0.4, 59.1+/-0.4, 5.1+/-1.2), IM(++)+ATP(++)group (77.8, 55.5, 33.3, 44.4, 25.1+/-7.2, 8.4+/-0.5, 59.5+/-0.4, 6.5+/-1.1), IM(+++)+ATP(++) group (100.0, 100.0, 75.0, 62.5, 28.5+/-9.1, 8.9+/-0.5, 59.7+/-0.4, 7.6+/-0.7), IMII(b) group (100.0, 62.5, 75.0, 50.0, 27.3+/-10.3, 8.6+/-0.3, 59.5+/-0.4, 6.1+/-0.9); whereas the content of Zn, Cu in mitochondria and cAMP, SOD in gastric mucosa, and (3)H-TdR LCT of each group were showen as belows: normal control group (9.2+/-0.5, 58.3+/-0.3, 15.9+/-1.5, 170.5+/-6.1, 1079.7+/-227.4), CSG group (8.6+/-0.5, 57.8+/-0.3, 14.6+/-1.8, 163.3+/-5.6, 867.3+/-240.5), CAG group (8.3+/-0.4, 57.5+/-0.3, 13.4+/-1.8, 161.2+/-4.3, 800.9+/-221.8), CA group (8.9+/-0.4, 57.1+/-0.3, 10.2+/-3.9, 152.2+/-3.8, 325.7+/-186.8), ATP(++) group (9.1+/-0.4, 57.0+/-0.3, 12.4+/-1.8, 161.5+/-3.8, 642.9+/-174.3), IM(++)+ATP(++) group (8.6+/-0.4, 56.9+/-0.3, 12.0+/-2.3, 152.2+/-2.5, 326.3+/-160.3), IM(+++)+ATP(++) group (8.5+/-0.3, 56.8+/-0.2, 10.4+/-0.9, 147.4+/-2.6, 316.1+/-170.7), IMII(b) group (8.6+/-0.3, 56.9+/-0.3, 11.9+/-1.9, 150.0+/-2.8, 318.9+/-145.8), there were significant differences between groups (P<0.05-0.01). CONCLUSION: There was a significant difference between CG and GC in their ultrastructure and molecular biology. Only on the condition of changes of internal environment in combination with the harmful effect of external environment, chronic atrophic gastritis can then develop into gastric cancer. Hence it might have similar epithelial cell ultrastructure and molecular biological changes in ATP(++), IMII(b) and cancer, hence there were similar patterns of occurrence, development and transformation. Recognition of this trend might help to explore problems of prevention and cure.