促愈颗粒对大鼠乙酸胃溃疡愈合质量的影响

目的:观察促愈颗粒对大鼠乙酸胃溃疡愈合质量的影响.方法:用冰醋酸制备大鼠慢性胃溃疡模型,所有大鼠随机分为4组(空白模型组、促愈颗粒组、雷尼替丁组和正常对照组).HE染色观察大鼠愈合性胃溃疡再生黏膜腺体成熟度和炎症细胞浸润情况;硝酸还原法检测血清NO含量;放射免疫法检测血浆PGE2含量;免疫组织化学技术检测大鼠胃黏膜EGF的表达情况;透射电镜观察大鼠再生黏膜超微结构的变化.结果:给药28d后与模型组和雷尼替丁组比较,促愈颗粒组再生黏膜囊性扩张腺体数量及炎细胞数量明显减少(再生黏膜囊性扩张腺体数量:1.43±0.53 vs 3.84±1.08.2.36±0.79,P<0.01和P<0.05;炎细胞数量:9.92±2.66 vs 28.32±6.96,17.92±4.76,P<0.01和P<0.05);血清NO及血浆PGE2含量显著增高(NO:105.41±8.02μmol/g vs 67.35±16.85,79.1 8±28.05μmol/g,P<0.0 1或P<0.05;PGE2:125.50±11.95 ng/L vs 97.33±11.84,118.83±13.25 ng/L,P<0.01和P>0.05);胃黏膜EGF表达明显增强(25.38±5.17 vs 16.82±2.13,21.12±6.08,P<0.05和P<0.05);促愈颗粒组超微结构的恢复亦优于模型组和雷尼替丁组.结论:促愈颗粒能提高溃疡再生黏膜结构,功能成熟度及电镜下成熟度,从而提高溃疡愈合质量.     

柴胡桂枝汤对大鼠乙酸胃溃疡愈合质量的影响

目的研究柴胡桂枝汤对大鼠乙酸胃溃疡愈合质量的影响。方法用冰醋酸制备大鼠慢性胃溃疡模型,随机分为A、B、C三组,分别灌服柴胡桂枝汤、西咪替丁、生理盐水。用苏木精-伊红染色和粘液组织化学染色对大鼠愈合性胃溃疡再生粘膜进行定量观察。用硝酸还原酶法检测胃粘膜NO含量。结果柴胡桂枝汤组和西咪替丁组再生粘膜厚度、粘液指数高于生理盐水组(P＜0.01),粘膜肌层缺损宽度小于生理盐水组(P＜0.01),NO含量高于生理盐水组(P＜0.01～0.05);柴胡桂枝汤组粘液指数及NO含量高于生理盐水组(P＜0.01～0.05)。结论柴胡桂枝汤能提高溃疡愈合质量,是临床抗消化性溃疡复发的可能机制之一。     

壳聚糖对胃溃疡愈合质量影响的实验研究

背景：消化性溃疡是临床常见病且易复发，溃疡愈合质量与其复发有密切关系。目的：研究壳聚糖对大鼠胃溃疡愈合质量的影响及其可能机制。方法：大鼠随机分为空白对照组、两组药物对照组（硫糖铝和雷尼替丁）和三组实验组（壳聚糖、壳聚糖＋硫糖铝或雷尼替丁）。给药14天后测量溃疡面积并行HE染色、AB—PAS、第Ⅷ因子和SP法免疫组化染色，测定一系列溃疡愈合质量指标以及表皮生长因子（EGF）、碱性成纤维细胞生长因子（bFGF）和诱生型一氧化氮合酶（iNOS）的表达。结果：实验组溃疡面积较空白对照组和药物对照组显著缩小（P〈0．01）；再生黏膜厚度较空白对照组增加，囊状扩张腺体数量减少，腺体层数增加，PAS阳性面积增加，肉芽组织中新生微血管数量增多（P〈0．01）。壳聚糖＋硫糖铝或壳聚糖＋雷尼替丁组的囊状扩张腺体数量显著小于雷尼替丁组（P〈0．05），腺体层数显著大于三者单用（P〈0．05），PAS阳性面积和新生微血管数量显著大于雷尼替丁组（P〈0．05）。各实验组EGF和bFGF的表达均显著高于空白对照组和雷尼替丁组（P〈0．05），但iNOS在各组间的表达无显著差异。结论：壳聚糖可提高大鼠胃溃疡愈合质量。其机制可能与增强EGF、bFGF的表达和促进肉芽组织中微血管增生有关。壳聚糖与硫糖铝和雷尼替丁对提高溃疡愈合质量具有协同作用。     

柴胡桂枝汤对大鼠乙酸胃溃疡愈合质量的影响

目的：研究柴胡桂枝汤对大鼠乙酸胃溃疡愈合质量的影响。方法：用冰醋酸制备大鼠慢性胃溃疡模型，随机分为Ａ、Ｂ、Ｃ三组，分别灌服柴胡桂枝汤、西咪替丁、生理盐水。用苏木精－伊红染色和粘液组织化学染色对大队愈合性胃溃疡再生粘膜进行定量观察。用硝酸还原酶法检测胃粘膜ＮＯ含量。结果：柴胡桂枝汤组和西咪替丁组再生粘膜厚度、粘液指数高于生理盐水组（Ｐ〈０．０１），粘膜肌层缺损宽度小于生理盐水组（Ｐ〈０．０１），ＮＯ     

胃灵颗粒对大鼠乙酸胃溃疡愈合质量的影响

目的 :研究胃灵颗粒对大鼠乙酸慢性胃溃疡愈合质量的影响。方法 :用冰醋酸制备大鼠乙酸慢性胃溃疡模型 ,随机分为 5组 ,分别灌服蒸馏水 ,雷尼替丁 ,低、中、高剂量胃灵颗粒 ,用苏木精 -伊红染色对大鼠愈合性胃溃疡再生粘膜进行定量观察 ,并测胃壁结合粘液量、胃酸、胃蛋白酶活性。结果 :胃灵颗粒组改善胃粘膜的组织损伤 ,并提高胃壁结合粘液量 ,减少胃酸的排出。结论 :胃灵颗粒能提高溃疡愈合质量 ,是临床抗消化性溃疡复发的可能机制之一。     

大鼠乙酸性胃溃疡复发模型的复制及健胃愈疡颗粒的干预作用

[目的]复制大鼠乙酸性胃溃疡复发模型并观察健胃愈疡颗粒（JWYY）的干预作用。[方法]采用改良Okabe乙酸涂抹法制作大鼠胃溃疡模型，腹腔注射白细胞介素1β（IL-1β）致愈合溃疡复发。44只大鼠随机分为正常对照组、假手术组、模型复发组、模型未复发组、JWYY组、奥美拉唑（OMLZ）组，观察各组胃溃疡复发率、胃蜜大体改变、胃窦组织病理学改变、炎症细胞密度计数。[结果]模型复发组胃溃疡复发率为87．50％，呈溃疡病理结构改变，溃疡边缘见残留之再生黏膜，再生黏膜较薄，有较多炎症细胞浸润。JwYY能改善胃溃疡愈合，减低IL-1β所诱导的瘢痕黏膜炎症细胞浸润的密度，降低溃疡复发率，与OMLZ无显著差别。[结论]IL-1β可能通过炎症细胞浸润诱导愈合的乙酸性胃溃疡复发；抑制炎症反应可能是JWYY抗溃疡复发的疗效机制之一。     

铝碳酸镁对实验性胃溃疡的疗效及其机制探讨

背景:铝碳酸镁已用于胃溃疡的治疗,但其具体机制尚不明确。目的:探讨铝碳酸镁对实验性胃溃疡大鼠的疗效及其作用机制。方法:建立实验性乙酸致大鼠胃溃疡模型,成模后分为对照组、铝碳酸镁低剂量组、铝碳酸镁高剂量组,分别给予0.9%Na Cl溶液、880 mg·kg~(-1)·d~(-1)和1 230 mg·kg~(-1)·d~(-1)铝碳酸镁灌胃。14 d后,行大体评估,以HE、CD31、VG染色评估再生黏膜组织成熟度,AB-PAS染色、氨基己糖水平、免疫组化染色和血清表皮生长因子(EGF)、前列腺素(PG)E_2评估功能成熟度。结果:与对照组相比,铝碳酸镁高剂量组溃疡指数(UI)明显降低(P0.05);铝碳酸镁低、高剂量组再生黏膜厚度增加(P0.05),囊状扩张腺体数量明显减少(P0.01),微血管密度(MVD)明显增加(P0.01),胶原纤维明显增多(P0.05);中性黏液分泌量和氨基己糖水平明显升高(P0.01),黏膜EGF、EGF受体(EGFR)和PGE_2表达均明显增强(P0.01),血清EGF、PGE_2水平明显升高(P0.01)。结论:铝碳酸镁能明显提高溃疡再生黏膜组织和功能的成熟度,提高溃疡愈合质量,其机制可能为中和胃酸,增强黏液-HCO3~-屏障,上调EGF、PGE_2表达。     

阿司匹林对大鼠胃溃疡愈合的影响及其机制

目的 探讨阿司匹林对胃溃疡的影响和机制.方法 用乙酸诱导大鼠胃溃疡,8 d后随机分为模型组、盐水组、阿司匹林组.用组织学方法检测溃疡形态、再生黏膜厚度,扩张腺体数,用免疫组化方法检测环加氧酶(COX)-1、COX-2、胃泌素在胃黏膜中的表达,用酶联免疫吸附测定法检测胃黏膜中的前列腺素E2(PGE2)含量,并检测胃液pH.结果 阿司匹林组的溃疡面积和扩张腺体数高于模型和盐水组(P<0.05),再生黏膜厚度低于模型和盐水组(P<0.05);阿司匹林组COX-2、胃泌素积分光密度高于模型和盐水组(P<0.01);阿司匹林组的PGE2含量和胃液pH低于模型和盐水组(P<0.01).结论阿司匹林抑制COX活性使PGE2生成减少,引起胃泌素分泌增加,胃酸分泌增多,加重溃疡.     

七方胃痛胶囊对大鼠乙酸胃溃疡愈合质量的影响

[目的]观察七方胃痛胶囊对大鼠实验性胃溃疡愈合质量(QOUH)的影响.[方法]予冰醋酸注射制作大鼠胃溃疡模型后,随机分为5组:分别予0.85%氯化钠液、雷尼替丁胶囊、七方胃痛胶囊(小、中、大3个剂量),连续灌胃14 d,处死大鼠,制作病理切片,予苏木精-伊红染色和黏液组织化学染色,在光镜下观察溃疡指数、再生黏膜厚度、黏膜肌层缺损宽度、表面黏液厚度、再生组织结构.[结果]七方胃痛胶囊能增加再生黏膜厚度及表面黏液厚度,减少再生黏膜肌层缺损宽度(P＜0.01),有量效关系(P＜0.01),能明显改善再生组织结构.[结论]七方胃痛胶囊能改善再生组织结构,从而提高QOUH,达到抗溃疡复发的作用.     

促愈颗粒对胃溃疡实验大鼠胃黏膜表皮生长因子及其受体表达的影响

[目的]研究促愈颗粒对乙酸烧灼型胃溃疡(GU)大鼠胃黏膜表皮生长因子(EGF)及其受体(EGFR)表达的影响。[方法]将大鼠随机分为4组:正常对照组,模型组,促愈颗粒组和雷尼替丁组。乙酸制备慢性GU大鼠模型后,于给药14 d和28 d后分2次处死大鼠,观察胃黏膜组织形态,免疫组织化学技术检测大鼠胃黏膜EGF及EGFR水平。[结果]与模型组比较,促愈颗粒组和雷尼替丁组囊状扩张腺体数量均显著减少(P<0.01,<0.05),EGF及EGFR水平均显著增高(P<0.01,<0.05),且促愈颗粒组作用均优于雷尼替丁组(均P<0.05)。[结论]促愈颗粒可能通过增加胃黏膜EGF和EGFR的水平,进而提高GU再生黏膜结构和功能成熟度,从而促进溃疡愈合,提高溃疡愈合质量,并防止溃疡复发。     

柴胡桂枝汤对乙酸胃溃疡大鼠再生黏膜表层黏液的影响

[目的]探讨柴胡桂枝汤（CHGZT）改善溃疡愈合质量（QUH）的作用机制。[方法]对比观察大鼠乙酸胃溃疡形成后3个时间段再生黏膜表层黏液的分泌状态及CHGZT对其的影响。[结果]各组、各期再生黏膜黏液的分泌，不论是表层或黏膜内黏液，均较正常旺盛；与模型对照组相比，CHGZT 5d、30d再生黏膜表层黏液均明显增厚（P〈0．01）。[结论]增加再生黏膜表层黏液分泌可能是CHGZT改善QUH的作用机制之一。     

健脾理气颗粒对大鼠胃溃疡作用的研究

目的：研究健脾理气颗粒对大鼠胃溃疡及胃粘膜损伤的作用。方法：采用水浸应激致胃溃疡及口服乙醇致胃粘膜损伤法制模，再用健脾理气颗粒3个剂量组进行药效评价，并设对照组进行比较。结果：健脾理气颗粒3个剂量组对大鼠应激性胃溃疡的形成有明显的抑制作用（P＜0.05-0.01)，对口服乙醇致胃粘膜损伤也有保护作用，尤以10g/kg、20g/kg组为明显（P＜0.05-0.01)。结论：健脾理气颗粒具有明显地抑制大鼠胃溃疡及保护胃粘膜损伤作用。     

健胃汤抗大鼠乙酸胃溃疡及泼尼松再损伤的实验研究

目的 :从溃疡愈合质量 (QOUH )角度探讨健胃汤抗消化性溃疡 (PU )复发的可能机制。方法 :采用大鼠乙酸胃溃疡模型 ,观察健胃汤对该模型及泼尼松诱导的再损伤胃粘膜的影响 ,并测定其一氧化氮 (NO)、表皮生长因子 (EGF)的含量。结果 :健胃汤能改善胃粘膜的组织损伤并提高溃疡周围组织的 NO、EGF含量。结论 :健胃汤能提高 QOUH ,增强溃疡瘢痕处抗泼尼松再损伤能力 ;提高溃疡周围组织的 NO、EGF含量 ,这可能是其抗 PU复发的机制之一。     

Metabolism of oral trefoil factor 2 (TFF2) and the effect of oral and parenteral TFF2 on gastric and duodenal ulcer healing in the rat

BACKGROUND: Trefoil factors (TFFs) are peptides produced by mucus-secreting cells in the gastrointestinal tract. A functional association between these peptides and mucus, leading to stabilisation of the viscoelastic gel overlying the epithelia, has been suggested. Both oral and parenteral administration of the peptides increase the resistance of the gastric mucosa. AIM: To study the effect in rats of oral and parenteral porcine trefoil factor 2 (pTFF2) on the healing of gastric and duodenal ulcerations and to clarify the distribution and metabolism of orally administered pTFF2 in the gastrointestinal tract. METHODS: Gastric ulcers were induced in female Sprague-Dawley rats by indomethacin and duodenal ulcers by mercaptamine. The rats were treated for up to seven days with oral or subcutaneous pTFF2. Ulcer size after treatment was assessed by stereomicroscopy after whole mount staining with periodic acid-Schiff stain. (125)I-labelled pTFF2 was given orally to rats, and tissues were investigated by gamma counting of samples and by autoradiography of paraffin embedded sections. RESULTS: pTFF2 accelerated gastric ulcer healing after both oral and subcutaneous administration. Duodenal ulcers were aggravated by both treatments. After oral administration of (125)I-pTFF2, intact peptide was recovered from the superficial part of the mucus layer in the stomach; it passed through the small intestine but was degraded in the caecum. Only a minor part of the labelled pTFF2 entered the colon and was excreted in the faeces. Most of the label was excreted in the urine. CONCLUSIONS: Oral as well as parenteral pTFF2 accelerates the healing of gastric ulceration and aggravates duodenal ulcers. Oral pTFF2 binds to the mucus layer of the stomach and the small intestine but does not reach the colonic mucosa.     

Influence of gender difference and gastritis on gastric ulcer formation in rats

BACKGROUND: Male patients with gastritis are found to have a high risk of developing peptic ulcer diseases. However, how gastritis or gender difference affects gastric ulcer formation is unclear. The present study aimed to investigate the relationship between ethanol-induced acute gastritis and gastric ulcer formation in rats. METHODS: Acute gastritis or gastric ulcer was induced in the rat stomach by 80% ethanol or 60% acetic acid, respectively. Rats were killed either with gastritis alone or thereafter at day 1, 3 or 6 after ulcer induction. The number of proliferating and apoptotic cells, the mucosal mucus and prostaglandin E(2) (PGE(2)) level were also determined. RESULTS: Male rats with acute gastritis potentiated gastric ulcer formation, while gastritis in female rats prevented ulceration. Female rats with gastritis had a significantly faster ulcer-healing rate. More apoptotic cells were found in the gastritis groups, but only the female gastritis group produced more proliferating cells and had a decrease in the apoptosis-over-proliferation ratio. The mucus level was higher in female rats after ulcer induction. Mucosal PGE(2) level was higher in female rats with acute gastritis. Both mucus and PGE(2) were increased during ulcer healing in both genders. CONCLUSIONS: This study shows that gender difference plays a role in the pathogenesis of ulcer formation. The number of cells with apoptosis or proliferation determines, in part, the gender difference on gastric ulcer formation in rats. Gastric PGE(2) not only contributes to this process, but also together with gastric mucus participates in the ulcer-healing process in the stomach.     

Carcinogenic Action of 2,7-Diacetylaminofluorene on the Stomach of Rats with Experimental Gastric Ulcer

Penetrating ulcers of gastric glandular mucosa were produced in male Buffalo rats by thermocautery. These rats, and uninjured control animals, were fed with a diet containing a known carcinogen, 2,7 diacetylaminofluorene (2,7-DAAF). The purpose of this study was to find whether the presence of gastric ulcer will enhance the incidence of gastric carcinoma. In 14% of rats in which gastric ulcers were associated with the exposure to oral carcinogen, gastric adenocarcinomas were found. No gastric tumors were diagnosed in rats having uninjured gastric mucosas prior to the ingestion of carcinogen. It is concluded that the contact of chemical carcinogen 2,7-DAAF with injured, healing gastric mucosa, enhanced the malignant transformation of gastric cellular elements. Under the conditions of this experiment, the presence of gastric ulcer contributed to the appearance of gastric adenocarcinoma.     

Epidermal Growth Factor in Gastric Ulcer Healing by Nocloprost,a Stable Prostaglandin E2 Derivative

Background: The gastroprotective and ulcer-healing properties of prostaglandins, especially in gastric ulcers induced by non-steroidal anti-inflammatory drugs, are well established. Ulcer healing is an active process of filling the mucosal defect with migrating and proliferating epithelial cells combined with angiogenesis in granulation tissue at the ulcer bed. Growth factors, especially epidermal growth factor (EGF) and transforming growth factor alpha (TGFa) are crucial in the regulation of the reconstruction of damaged mucosal structures. Methods: In this double-blind, randomized, prospective study 40 patients with gastric ulcer were treated with nocloprost, a stable prostaglandin E₂ derivative, or with ranitidine. All subjects underwent endoscopy before and after 4 and 8 weeks of anti-ulcer therapy. During endoscopy mucosal biopsies were performed for determination of EGF content in gastric mucosa at the ulcer margin and in the intact mucosa. Additionally, EGF output in saliva and its plasma concentrations were determined in all subjects before and during the treatment. Results: The gastric ulcer healing rate after 4 weeks was significantly higher in patients treated with nocloprost than in those treated with ranitidine (63% versus 39%, respectively). At initial examination the EGF content in the gastric mucosa obtained from the ulcer edge was significantly higher than that in the intact mucosa. There was a significant increase in the EGF content in both the ulcer margin and the intact mucosa in subjects treated with nocloprost but not in patients under treatment with ranitidine. Similarly, patients treated with nocloprost had significantly higher EGF output in saliva and higher EGF concentration in plasma throughout the anti-ulcer therapy. Conclusion: Nocloprost is superior to ranitidine in the treatment of chronic gastric ulcers, and these effects could be due, at least in part, to higher expression and mucosal content of EGF in the ulcer area.     

芍甘海贝蒲术汤抗胃溃疡作用的实验研究

目的 :研究芍甘海贝蒲术汤对实验性胃溃疡的防治作用 ,并探讨其作用机制。方法 :观察预先应用中药对应激、乙醇及幽门结扎所诱发的胃粘膜损伤的影响 ;并观察连续应用中药 14d后醋酸性胃粘膜损伤的愈合情况 ;同时检测胃液量、总酸度、胃蛋白酶活性、胃壁结合粘液、胃粘膜超氧化物歧化酶 (SOD)、丙二醛 (MDA)及脑组织和胃粘膜的一氧化氮合酶 (NOS)的含量。结果 :芍甘海贝蒲术汤显著抑制应激、乙醇及幽门结扎性胃粘膜损伤 ,加速醋酸性胃溃疡的愈合 (P<0 .0 5 ,<0 .0 1) ;抑制胃液分泌和胃蛋白酶活性 ,显著增加胃粘膜组织 SOD、NOS含量 ,减低 MDA的生成 (P<0 .0 5 ,<0 .0 1)。结论 :芍甘海贝蒲术汤可能通过增强胃粘膜的细胞保护作用而产生抗胃溃疡的效应。