Ultrastructural observation of the gastric mucosa in chronic gastritis patients treated by traditional Chinese medicine

AIM: To demonstrate the relationship between the ultrastructural changes of the gastric mucosa and the syndrome differentiation in chronic gastritis.METHODS: Sixteen chronic gastritis patients with Piweixuhan (PXG, the cold of insufficiency syndrome of the spleen and the stomach) and fifteen chronic gastritis patients with Ganweibuhe (GBG, incoordination syndrome of the liver and the stomach) were treated with Jianpiwenwei decoction (JWD, invigorating the spleen and warming the stomach) or Shuganhewei decoction (SHD, dispersing the stagnated Liver Qi and regulating the stomach), respectively for three months. Before and after treatment, a gastroscopy was performed and the gastric mucosa was collected from the lesser curvature of the antrum of each patient. The ultrasections were observed and photographed under the JEM-100C X electron microscope.RESULTS: The common ultrastructural anomalies of the two types of chronic gastritis were the plasmacyte infiltration and the lesions of the mucosal epithelial cells, chief cells and antral mucous cells. There were obvious differences between the two types. In PXG, the predominant lesion of the chief cells was swelling of the mitochondria, while in GBG the rough endoplasmic reticulum was enlarged in the chief cells and the plasmacytes. After treatment, most cases of the ultrastructural lesions reverted to normal or improved.CONCLUSION: There was a close relationship between the ultrastructural changes of gastric mucosa and the syndrome differentiation of chronic gastritis. JWD and SHD could significantly improve the ultrastructural lesions of the gastric mucosa.     

Ultrastructural research on chronic gastritis treated by traditional Chinese medicine

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Characteristic features of ghrelin cells in the gastrointestinal tract and the regulation of stomach ghrelin expression and production

Ghrelin was isolated as an endogenous ligand for the GH secretagogue receptor from the rat stomach. Although physiological effects of ghrelin have been revealed by numerous studies, the regulation of stomach ghrelin remains obscure, and the factor that directly regulates ghrelin expression and production has not been identified. Here, we show some data regarding the characteristic features of ghrelin cells and the regulation of stomach ghrelin. In the gastrointestinal tract, ghrelin cells were identified as opened- and closed-type cells, and it was found that the number of ghrelin cells decreased from the stomach to the colon. The postnatal change in number of ghrelin cells in the stomach showed a sexually dimorphic pattern, indicating a role of estrogen in the regulation of stomach ghrelin. In vitro studies revealed that estrogen stimulated both ghrelin expression and production and that treatment with formestane, an aromatase （estrogen synthetase） inhibitor, decreased ghrelin expression level. On the other hand, leptin was found to inhibit both basal and estrogen-stimulated ghrelin expression. Moreover, both aromatase mRNA- expressing cells and leptin cells were found to be located close to ghrelin cells in the gastric mucosa. Furthermore, we found an inverse relationship between gastric ghrelin and leptin levels in a fasting state, and we revealed relative changes in expression of gastric ghrelin, estrogen and leptin in the postnatal rats. We propose that gastric estrogen and leptin directly regulate stomach ghrelin and that the balance control through gastric estrogen and leptin contributes to the altered ghrelin expression level in some physiological states.     

Atrial natriuretic peptide signal pathway upregulated in stomach of streptozotocin-induced diabetic mice

AIM:To investigate atrial natriuretic peptide(ANP) secretion from gastric mucosa and the relationship between the ANP/natriuretic peptide receptor type A (NPR-A)pathway and diabetic gastroparesis. METHODS:Male imprinting control region(ICR)mice (4 wk old)were divided into two groups:control mice, and streptozotocin-induced diabetic mice.Eight weeks after injection,spontaneous gastric contraction was recorded by using physiography in control and streptozotocin-induced diabetic mice.The ANP-positive cells in ...     

十二指肠胃反流对大鼠胃黏膜细胞凋亡及相关细胞因子表达的影响

目的研究十二指肠胃反流(duodenogastric reflux,DGR)对大鼠胃黏膜细胞凋亡及相关细胞因子表达的影响,探讨DGR胃黏膜损伤机制。方法手术组成年SD大鼠10只用于制备和收集十二指肠混合液。DGR模型组和对照组各取SD大鼠8只,前者十二指肠液灌胃,后者生理盐水灌胃。2周后处死大鼠。采用TUNEL技术观察胃黏膜细胞凋亡情况。采用免疫组化方法分析胃黏膜组织TNF-α、ET-1和NOS-2的表达。结果 DGR模型大鼠胃黏膜病理提示造模成功。DGR模型组胃黏膜凋亡细胞在黏膜全层均可见,凋亡指数(AI)显著高于对照组(P<0.05)。DGR模型组大鼠胃黏膜细胞的TNF-α、ET-1和NOS-2的表达均明显高于对照组(P<0.05)。结论细胞凋亡与TNF-α、ET-1和NOS-2等细胞因子表达异常可能参与DGR胃黏膜损伤乃至细胞癌变的发病机制。     

中医药辨证论治慢性胃炎动物的超微结构观察

观察慢性胃炎脾胃虚寒型、肝胃不和型两种大鼠模型分别用健脾温胃汤、疏肝和胃汤治疗前后胃粘膜的超微结构改变，结果表明，中医药辨证论治能明显地改善实验大鼠慢性胃炎的超微结构损伤。     

Atrial natriuretic peptide signal pathway upregulated in stomach of streptozotocin-induced diabetic mice

AIM:To investigate atrial natriuretic peptide(ANP) secretion from gastric mucosa and the relationship between the ANP/natriuretic peptide receptor type A (NPR-A)pathway and diabetic gastroparesis. METHODS:Male imprinting control region(ICR)mice (4 wk old)were divided into two groups:control mice, and streptozotocin-induced diabetic mice.Eight weeks after injection,spontaneous gastric contraction was recorded by using physiography in control and streptozotocin-induced diabetic mice.The ANP-positive cells in ...     

TFF2在胃癌、癌旁及正常胃黏膜组织中的表达及其与血管生成的关系

目的:探讨三叶因子2(TFF2)、血管内皮生长因子(VEGF)和微血管密度(MVD)在胃癌发生、发展、浸润和转移中的作用.方法:选取广西医科大学第一附属医院2008-01/2009-06接受胃大部切除术的胃癌标本50例,采用SP免疫组织化学方法检测30例正常胃黏膜组织、50例癌旁组织和50例胃癌组织中TFF2、VEGF...     

Effect of scorpion toxin on the enterochromaffin-like cells in normal and Trypanosoma cruzi-infected rats: a morphological study

Intravenous injection of scorpion toxin (Tityus serrulatus) in normal and Trypanosoma cruzi infected rats did not cause ultrastructural morphologic changes on enterochromaffin-like (ECL) cells of the stomach, although it induced a significant increase of the gastric secretion. Our data seem to indicate that gastric ECL cells structure is not affected by stimulation with scorpion toxin or by acute infection with T. cruzi in the rat.     

硫氧还蛋白-1在急性坏死性胰腺炎并急性胃黏膜损伤中的作用

目的探讨硫氧还蛋白-1（TRX-1）在实验性急性坏死性胰腺炎（ANP）并急性胃黏膜损伤发病机制中的作用以及抗氧化剂褪黑素对其的影响。方法72只大鼠随机分为对照组（C组,n=24）、ANP组（A组,n=24）和褪黑素干预组（M组,n=24）。A组分3次腹腔内注射6％L-精氨酸（L—Arg）1．5g／kg建立ANP模型;C组同法注射等量生理盐水;M组于首次注射L—Arg前0．5h腹腔内注射1％褪黑素50μg／kg。各实验组大鼠于末次腹腔内注射后6h、12h和24h分批处死。光镜下观察胰腺和胃组织并进行病理学评分,采用免疫组化检测TRX-1在胃黏膜的表达,并检测胃黏膜中MDA、MPO的含量。结果A组各时点胃黏膜TRX-1的染色积分及MDA、MPO的含量明显高于C组（P均〈0．05）;M组各时点胃黏膜中TRX一1的染色积分及MDA、MPO的含量明显低于A组（P均〈0．05）,胰腺和胃组织病理改变较A组明显减轻（P均〈0．05）。结论内源性的TRX-1可能是胃黏膜组织抵御氧化应激损伤的重要因子之一,TRX-1的表达量可能与组织氧化应激损伤的严重程度有关。外源性的褪黑素在ANP时可能通过其抗氧化作用,减轻胃黏膜氧化应激损伤的程度,对胃黏膜有一定的保护作用。     

Aspartic proteinases in gastric mucosa of the rat: absence of pepsinogen I, genetic polymorphism of pepsinogen II, and presence of slow-moving proteinase

We have examined relationships among the aspartic proteinases in rat and human gastric mucosa by electrophoretic analysis in polyacrylamide gel and by immunoblotting and immunohistochemical staining using rabbit antisera to human pepsinogen I (PG I), pepsinogen II (PG II), and slow-moving proteinase. By electrophoretic analysis, the major proteolytic bands in mucosal extracts from each of three strains of rats had rates of anodal migration that were similar to the fastest migrating isozymogens of human PG I. However, immunoblots revealed that these bands and several minor proteolytic bands with slower rates of anodal migration reacted with antiserum to PG II. Two proteolytic bands in rat gastric mucosa that migrated concurrently with human slow-moving proteinase reacted with antihuman slow-moving proteinase reacted with antihuman slow-moving proteinase. None of the proteolytic bands in rat gastric mucosa reacted with anti-PG I. By immunohistochemical staining, anti-PG I failed to stain any cells in rat fundic gland or antral mucosa. By contrast, anti-PG II stained mucus neck and chief cells in fundic gland mucosa and pyloric gland cells in antral mucosa, and anti-slow-moving proteinase stained surface and foveolar epithelial cells throughout the stomach. The results indicate that the gastric mucosa of the rat does not contain PG I.     

胃癌组织碱性成纤维细胞生长因子表达及对血管新生和肿瘤进展的影响

目的　探讨碱性成纤维细胞生长因子 (bFGF)在胃癌组织中表达及其对血管新生和肿瘤生物学行为的影响。方法　应用免疫组化SP法检测 74例胃癌 ,17例癌旁组织bFGF表达及间质微血管密度 (MVD)。结果　胃癌组织中肿瘤细胞、间质新生血管高度表达bFGF。癌组织bFGF表达(77.0 3% )明显高于癌旁组织 (2 9.4 1% ,P <0 .0 1)。癌旁胃黏膜及伴有肠上皮化生的胃黏膜表达bFGF较弱。bFGF高表达组的平均MVD值 (79.3± 11.2 )明显高于bFGF低表达组 (71.2± 11.9,P <0 .0 5 )。此外bFGF表达程度与胃癌淋巴结转移和癌浸润深度密切相关。结论　bFGF可促进肿瘤间质微血管生成 ,加速肿瘤浸润和转移。     

Ghrelin, a novel growth hormone-releasing acylated peptide, is synthesized in a distinct endocrine cell type in the gastrointestinal tracts of rats and humans

Ghrelin, a novel GH-releasing acylated peptide, was recently isolated from rat stomach. It stimulated the release of GH from the anterior pituitary through the GH secretagogue receptor (GHS-R). Ghrelin messenger RNA and the peptide are present in rat stomach, but its cellular source has yet to be determined. Using two different antibodies against the N- and C-terminal regions of rat ghrelin, we identified ghrelin-producing cells in the gastrointestinal tracts of rats and humans by light and electron microscopic immunohistochemistry and in situ hybridization combined with immunohistochemistry. Ghrelin-immunoreactive cells, which are not enterochromaffin-like cells, D cells, or enterochromaffin cells, accounted for about 20% of the endocrine cell population in rat and human oxyntic glands. Rat ghrelin was present in round, compact, electron-dense granules compatible with those of X/A-like cells whose hormonal product and physiological functions have not previously been clarified. The localization, population, and ultrastructural features of ghrelin-producing cells (Gr cells) indicate that they are X/A-like cells. Ghrelin also was found in enteric endocrine cells of rats and humans. Using two RIAs for the N- and C-terminal regions of ghrelin, we determined its content in the rat gastrointestinal tract. Rat ghrelin was present from the stomach to the colon, with the highest content being in the gastric fundus. Messenger RNAs of ghrelin and GHS-R also were found in these organs. Ghrelin probably functions not only in the control of GH secretion, but also in the regulation of diverse processes of the digestive system. Our findings provide clues to additional, as yet undefined, physiological functions of this novel gastrointestinal hormone.     

Uremia in the rat affects gastric cell growth and differentiation

The aim of this study was to determine if hypertrophy of different tissues seen in uremic rats included gastrointestinal hypertrophy and an increase in parietal cell mass that might explain the increased acid secretion we previously reported. Chronic renal failure was induced by subtotal nephrectomy. Despite a lower total body weight, uremic rats had a significantly greater stomach weight (33%), corpus area (13%), corpus mucosal height (19%), and parietal (32%) and enterochromaffin-like (ECL, 54%) cell density, but a 16% decrease in mucous neck cell region height. These findings suggest that uremia leads to gastric stem cell stimulation with differentiation favoring parietal and ECL cells over mucous cells. In addition, in uremic rats there was an increase in height of the duodenal mucosa, but not of the ileal or transverse colon mucosa. In conclusion, the present study shows that uremia in the rat promotes hypertrophy of the stomach with cell differentiation favoring parietal cells over mucus cells. The increase in parietal cell mass may explain the increased acid secretion in these rats.     

Histopathologic study on development and extension of atrophic change in the gastric mucosa

A histopathologic study was carried out on 30 resected stomachs with various gastric or duodenal diseases. Both the pyloric gland cells and the parietal cells were counted in serial sections of the surgically resected stomach. A good correlation (p less than 0.001) was found between the number of pyloric gland cells and parietal cells. The number of both glandular cells was greatest on the greater curvature and fewest at the part closer to the antrofundic mucosal border on the lesser curvature. In addition, a fairly uniform pattern was observed in the distribution of the parietal cells. The maximum density area of parietal cells was centered on the greater curvature of the stomach body, and this density decreased concentrically in proportion to the distance from the center. This uniform pattern was seen in almost all specimens, with or without atrophic change in the gastric mucosa. These results suggest that atrophic change does not develop in a particular part of the stomach but wholly and equally in the gastric mucosa.     

The effect of dexamethasone on gastric mucosal changes following sialoadenectomy in rat

In this study, dexamethasone-induced gastric lesions were studied in rats that had undergone sialoadenectomy. The ultrastructural changes developed during the study were detected by electron microscopically, while blood serum and stomach epidermal growth factor (EGF) concentrations were measured by RIA. The result of the study showed that gastric lesions were correlated with gastric mucus secretion and both serum and mucosa EGF levels. After the administration of dexamethasone, it was found that sialoadenectomy significantly (p<0.01) raised the incidence of stomach lesions (p<0.01), and a significant increase in mucus secretion was also found. Additionally, the serum and gastric mucosal EGF levels fell after sialoadenectomy when compared to normal rats. The most important gastric mucosal changes were observed in rats treated with dexamethasone and those both sialoadenectomised and treated with dexamethasone.     

Long-term omeprazole treatment suppresses body weight gain and bone mineralization in young male rats

BACKGROUND: The stomach is rich in endocrine cells, including those producing ghrelin, which is thought to play a role in the control of body growth. Omeprazole treatment is associated with hypergastrinaemia, resulting in growth of the oxyntic mucosa in general and the enterochromaffin-like (ECL) cells in particular. In the present study, we examined the effects of long-term omeprazole treatment on young male rats with respect to body growth and stomach. METHODS: Male rats (24 days old) were treated with omeprazole (400 micromol/kg/day) or vehicle for 77 days. The body weight was recorded twice per week. At sacrifice, dual-energy X-ray absorptiometry (DXA) was used to assess total bone area, bone mineral content (BMC), bone mineral density (BMD) and body composition (fat and lean body mass). The lengths of the spine and the femur were recorded. The plasma concentrations of gastrin and histamine were determined by radioimmunoassays. The endocrine cells of the stomach were examined by immunocytochemistry. RESULTS: The body weight gain was suppressed by omeprazole treatment. The bone area, BMC and BMD were reduced, while the lengths of the spine and the femur and the body composition were unchanged. Omeprazole-induced hypergastrinaemia was associated with enlargement of the oxyntic area and with hyperplasia of ECL cells but not of A-like cells and D cells. In contrast, the enterchromaffin (EC) cell density in the antrum was reduced. CONCLUSIONS: Omeprazole treatment of young male rats reduces body weight and bone mass gain. The densities of ECL cells in the oxyntic mucosa was increased and of the EC cells in the antral mucosa reduced.