蛋壳提取物对实验性胃溃疡作用的研究

目的观察蛋壳提取物水剂对实验性大鼠胃溃疡的作用。方法制备大鼠应激性胃黏膜损伤模型、大鼠幽门结扎型胃溃疡模型、大鼠醋酸型胃溃疡模型,每种模型50只。分别用剂量为0.5,1.0,2.0 g/kg体重蛋壳提取物水剂及4.0 g/kg体重胃苏冲剂给予大鼠灌胃,对照组给予水灌胃,连用7 d。观察各药对应激型、幽门结扎型、醋酸型大鼠溃疡模型的影响。用碱滴定法测定胃液游离酸度、总酸度,用Anson法测定胃蛋白酶活性。结果与对照组相比,蛋壳提取物水剂可降低大鼠胃溃疡指数,减少溃疡面积,降低幽门结扎型胃溃疡胃液量、游离酸及总酸度,并降低胃蛋白酶活性（P〈0.01）。结论蛋壳提取物水剂具有抗实验性胃溃疡的作用,尤其对老年大鼠效果显著。     

萎胃康颗粒剂治疗慢性萎缩性胃炎的实验研究

[目的]观察萎胃康颗粒剂对慢性萎缩性胃炎（CAG）的治疗作用,为临床治疗和应用提供实验依据。[方法]用多重刺激复制CAG模型。以三九胃泰作为阳性对照药,运用光镜和电镜观察萎胃康颗粒剂对模型大鼠胃黏膜病理变化的影响。[结果]萎胃康颗粒剂能明显改善胃黏膜的萎缩状况,与阳性对照组比较差异有统计学意义（P〈0.05）。[结论]该方药治疗CAG具有良好的作用。     

萎平舒胶囊治疗慢性萎缩性胃炎实验研究

目的 :探讨萎平舒胶囊治疗慢性萎缩性胃炎 (CAG)的作用机制。方法 :采用综合法制备大鼠 CAG模型 ,设正常对照组、模型组、三九胃泰阳性对照组以及萎平舒胶囊治疗组 ,观察大鼠体重、胃液中游离酸和胃蛋白酶活性以及胃粘膜病理组织学改变。结果 :萎平舒治疗 6 0 d,与模型组比较 ,大鼠的体重差异无显著改变 ;胃液游离酸显著升高 (P <0 .0 5 ) ,胃蛋白酶活性升高 ,但无统计学差异 ;能明显改善胃粘膜上皮细胞形态异常及腺体萎缩 ,使血管扩张完全消除 ,胃粘膜炎细胞浸润显著减少 ,变薄的胃粘膜显著增厚趋向正常。结论 :萎平舒胶囊对 CAG具有较好的治疗作用     

欣胃颗粒对慢性萎缩性胃炎大鼠胃黏膜病理形态学及胃液pH影响的研究

[目的]探讨欣胃颗粒治疗慢性萎缩性胃炎(CAG)的疗效及其机制.[方法]采用100 μg/ml甲基硝基亚硝基胍(MNNG)自由饮用,0.3 g/kg雷尼替丁喂养,配合饥饱失常等综合方法进行造模,3个月制成大鼠CAG模型.设正常、模型、维酶素组及欣胃颗粒高、中、低剂量治疗组,观察大鼠胃黏膜病理形态学及胃液pH变化.[结果]各药物治疗组大鼠胃黏膜均有不同程度改善,欣胃颗粒高、中、低剂量组与模型组、维酶素组比较,pH值明显降低(P＜0.05,或＜0.01).[结论]欣胃颗粒通过改善胃黏膜的病理形态,从而促进胃酸分泌治疗CAG.     

益胃冲剂对大鼠慢性萎缩性胃炎及胃癌前病变的逆转作用

为了验证益胃冲剂治疗慢性萎缩性胃炎的逆转作用，本实验复制了大鼠慢性萎缩性胃炎模型，从胃粘膜病理变化，胃粘膜跨膜电位差（ＰＤ），胃液ｐＨ值及胃蛋白酶活性等方面加以观察．１材料和方法１．１材料♂ＳＤ大鼠，体重１８０ｇ±２０ｇ；益胃冲剂（黄芪、党参、生地、...     

萎胃颗粒对慢性萎缩性胃炎大鼠胃黏膜核因子-κB和内源性抑制因子表达的影响

[目的]探讨萎胃颗粒对慢性萎缩性胃炎(CAG)大鼠核因子(NF)-κB及其内源性抑制因子(IκBα)表达的影响,进一步明确其作用机制.[方法]采用综合法复制大鼠CAG模型,造模成功后随机分为正常组、模型组及萎胃颗粒低、中、高剂量组,每组10只,观察萎胃颗粒对CAG大鼠胃黏膜NF-κB和IκBa表达的影响.[结果]NF-κB蛋白NF-κBOD值正常组为0.116±0.033,模型组0.183±0.035,萎胃颗粒低剂量组0.158±0.031,中剂量组0.144±0.039,高剂量组0.126±0.036.与模型组比较,萎胃颗粒各治疗组NF-κBOD值均有明显下降(P＜0.01),且这种作用呈剂量依赖性:低剂量组＞中剂量组＞高剂量组,3组比较差异有统计学意义(P＜0.01).IκBα蛋白OD值正常组为4.25±1.02,模型组为2.08±0.74,萎胃颗粒低剂量组2.77±0.78,中剂量组3.46±0.84,高剂量组4.12±0.96.与模型组比较,萎胃颗粒各治疗组IκBαOD值均有明显的升高(P＜0.01),且这种作用呈剂量依赖性:低剂量组＜中剂量组＜高剂量组,3组比较差异有统计学意义(P＜0.01).[结论]萎胃颗粒可能通过增加CAG大鼠胃黏膜IκBα的表达,促进IκBα与NF-κB结合,进而抑制NF-κB的活化,降低胃黏膜炎症程度,从而有效抑制胃黏膜的增生,避免CAG进一步向胃癌转化.     

萎胃颗粒对大鼠萎缩性胃炎模型COX-2和p53表达的影响

[目的]探讨萎胃颗粒对慢性萎缩性胃炎(CAG)大鼠模型COX-2和p53表达的影响。[方法]选取90只SD雄性大鼠随机分为6组(空白对照组、病理组、维酶素组、萎胃颗粒大剂量组、萎胃颗粒中剂量组、萎胃颗粒小剂量组),每组15只。对于病理组和4个治疗组进行CAG模型的复制,造模成功后,病理组、维酶素组、萎胃颗粒各剂量组分别给予相应的药物灌胃。治疗12周后,光镜下观察各组大鼠胃组织的病理损伤情况;并用免疫组化、ELISA等方法检测各组胃黏膜及血液中COX-2、p53表达情况。[结果]镜下可见CAG大鼠模型复制成功,且萎胃颗粒有治疗作用。免疫组化及ELISA试验显示空白组COX-2和p53呈弱表达;病理组COX-2和p53呈强阳性表达,显著高于空白组(P0.001);而萎胃颗粒3个不同剂量治疗组的COX-2和p53阳性表达均不同程度减弱,明显低于病理组(P0.001),且以大剂量组最为显著。[结论]萎胃颗粒能够调节CAG大鼠模型COX-2和p53表达,增强黏膜屏障的防御和修复能力,从而发挥对CAG的治疗作用。     

硫酸软骨素对鼠胃粘膜的保护作用研究

由冷冻－束缚应激、口服酸性乙醇及皮下注射利血平制备胃溃疡模型,观察硫酸软骨素（ＣＳ）对胃液分泌量、胃液酸度和胃蛋白酶活性的影响。结果：ＣＳ可抑制冷冻－束缚应激及利血平引起的胃粘膜损伤,认为ＣＳ对胃粘膜有良好的保护作用,可用于胃溃疡的治疗,且对大鼠胃液分泌量、胃液酸度和胃蛋白酶活性无明显影响。     

胃灵冲剂对大鼠慢性萎缩性胃炎黏膜G细胞及D细胞的影响

[目的]观察胃灵冲剂对大鼠慢性萎缩性胃炎（CAG）黏膜G细胞、D细胞的影响。[方法]120只Wistar雄性大鼠随机分为5组：正常对照组、模型组、维酶素组、胃灵冲剂小剂量组、胃灵冲剂大剂量组，除正常对照组外，其他大鼠制成CAG模型，模型制作成功后，对照组仅给予0．8s％氯化钠液灌胃，其他大鼠给予不同药物，30d后全部处死。应用免疫组织化学方法观察胃窦黏膜G细胞、D细胞数量。[结果]与正常对照组比较，模型组大鼠的O细胞、D细胞明显减少，与治疗组比较差异有统计学意K（P〈0．01）。[结论]G细胞、D细胞数量减少是CAG发生的重要因素之一，胃灵冲剂对胃黏膜的损害具有保护作用，是其有效治疗CAG的作用机制之一。     

胃痞消对实验性大鼠慢性萎缩性胃炎的作用

[目的]探讨健脾化瘀解毒复方胃痞消对慢性萎缩性胃炎(CAG)模型大鼠胃黏膜上皮细胞病理改变的影响.[方法]采用致癌化学物N-甲基-N'-硝基-N亚硝基胍配合饥饱失常、耗气泻下法建立CAG脾虚模型.采用免疫组化法检测胃黏膜萎缩、肠上皮化生等病理变化.[结果]模型对照组胃黏膜萎缩、肠化生均较正常组明显增加(P＜0.01);胃痞消预防组、高、中、低剂量组较模型对照组明显降低(均P＜0.01).[结论]胃痞消防治CAG的作用机制与其通过降低胃黏膜萎缩、肠化生及两者并见出现率,逆转已发生的萎缩,从而阻止其发生癌变.     

高良姜油抗实验性胃溃疡作用及其机制研究

[目的]研究高良姜油抗胃溃疡（GU）的作用及其机制。[方法]ICR小鼠随机分成7组,分别为：正常对照组,模型组,奥美拉唑组（0.014 g/kg）,良附丸组（2 g/kg）,高良姜油高、中、低剂量（8、42、ml/kg）组,预防给药6d后,采用利血平致GU小鼠模型,收集小鼠胃液,测定胃液量、总酸度、胃蛋白酶活性及血清一氧化氮（NO）、超氧化物歧化酶（SOD）及丙二醛（MDA）水平。[结果]与模型组相比,高良姜油高、中剂量组,良附丸组,奥美拉唑组均能抑制利血平致GU小鼠模型胃液量、总酸度及胃蛋白酶活性,且能增加血清NO水平和SOD活性,降低MDA水平;但中剂量组胃蛋白酶活性变化无统计学意义。[结论]高良姜油抗GU作用机制可能与其抑酸、抗氧化、增强保护因子有关;高良姜油高剂量抗氧化与增加血清NO水平的作用与良附丸相当。     

Protective effect of glucosamine against ibuprofen-induced peptic ulcer in rats

BACKGROUND: Helicobacter pylori is the major causative factor of ulcer but the use of ibuprofen and other non-steroidal anti-inflammatory drugs have also been implicated in development of ulcer. The purpose of the present study was to determine the anti-ulcer effect of glucosamine. METHODS: The protective effect of glucosamine on ibuprofen-induced peptic ulcer in male albino rats was studied with respect to changes in the volume of gastric juice, acid output, pepsin activity, activities of membrane bound ATPases, protein content, glycoprotein components and histopathology. RESULTS: Oral administration of ibuprofen caused significant increase in the number of lesions in the gastric mucosa, increases in the volume of gastric juice and acidity, and decreased activity of pepsin. The levels of protein content and glycoprotein components (hexose, hexosamine and sialic acid) and ATPase activities were also observed. Oral pretreatment with glucosamine resulted in significant reduction in the number of lesions in the gastric mucosa and decreases in the volume of gastric juice and acidity. The pepsin activity was also maintained at near normalcy. Prior oral administration of glucosamine significantly prevented the ibuprofen-induced depletion of protein and glycoprotein components and maintained the activities of membrane bound ATPases as compared to untreated ulcer induced group of rats. CONCLUSION: The anti-ulcerogenic activity of glucosamine might be ascribable to its ability to neutralize the hydrochloric acid secreted into the stomach and to its capability to strengthen the mucosal barrier by increasing mucosal glycoprotein synthesis and to its free radical scavenging property. Histopathological investigations of the mucosal tissue also support the anti-ulcerogenic effect of glucosamine.     

Inhibition of peptic activity by carbenoxolone and glycyrrhetinic acid

Carbenoxolone (Biogastrone, Berk) has been shown to reduce the peptic activity and total acidity of gastric juice obtained from anaesthetized pylorus-ligated rats without affecting significantly the volume of gastric juice secreted or the K(+) concentration. Glycyrrhetinic acid was less potent in reducing peptic activity and caused no reduction in total acidity.Antipeptic activity of carbenoxolone has also been demonstrated in vitro using the pepsin plate technique and the haemoglobin pepsin assay.It is suggested that these actions of carbenoxolone may contribute to the increased rate of healing of peptic ulcer in patients treated with the drug.     

Species and strain differences in mepirizole-induced duodenal and gastric lesions

Species and strain differences in mepirizole-induced duodenal and gastric lesions were studied. Mepirizole at 200 mg/kg given orally induced deep duodenal ulcers and gastric erosions in nonfasted Sprague-Dawley, Fisher, Wistar, and Donryu rats at an incidence of over 75%. Mepirizole at 300 mg/kg given orally also induced penetrating duodenal ulcers in nonfasted rabbits at an incidence of 50%. There was little or no damage to the duodenum and stomach in mice and dogs given 200–300 mg/kg of mepirizole orally or subcutaneously. The stomachs of fasted guinea pigs given 200 mg/kg of mepirizole had superficial erosions at a high incidence (93.3%). Mepirizole at 200 mg/kg given intraduodenally significantly reduced the volume of gastric juice but increased the acidity and pepsin activity in both pylorus-ligated and acute fistula rats. In chronic fistula rabbits, however, the agent at 200 mg/kg given orally reduced the volume and acidity, but increased the pepsin activity. The mechanism of duodenal ulceration by mepirizole differs slightly in rats and rabbits.     

萎胃汤治疗慢性萎缩性胃炎伴癌前病变临床疗效及对PCNA和bal-2、bax表达的影响

[目的]探讨萎胃汤治疗慢性萎缩性胃炎(CAG)的临床疗效及对胃黏膜增殖细胞核抗原(PCNA)和bcl-2、bax表达的影响.[方法3200例CAG患者随机分为萎胃汤治疗组与胃复春对照组,分别治疗2个疗程后对比观察疗效,并对2组伴肠化生(IM)、不典型增生(ATP)的患者,采用免疫组化(S-P)法和凋亡细胞原位检测(TU...     

愈疡1号颗粒对胃溃疡大鼠自由基代谢相关因素的影响

[目的]探讨愈疡1号颗粒对胃溃疡（Gu）大鼠自由基代谢相关因素表达的影响。[方法]应用冰乙酸注射法建立大鼠GU模型,随机分为5组,即正常组、模型组、奥美拉唑组及愈疡1号颗粒高、低剂量（高、低剂量）组,给予相应干预后测定各组大鼠胃黏膜丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH—Px）、一氧化氮（N0）的表达及血清NO水平。[结果]模型组大鼠胃黏膜MDA、NO水平均较正常组显著升高,SOD、GSH—Px活性均较正常组显著降低。与模型组比较,高、低剂量组均能够明显提高大鼠胃黏膜SOD、GSH—Px活性,明显降低MDA、NO水平。高剂量组能明显降低血清NO水平。[结论]愈疡1号颗粒通过降低胃黏膜MDA、NO表达及血清NO水平,提高胃黏膜SOD和GSH-Px的表达,起到保护胃黏膜的作用,是其治疗GU的重要机制之一。     

萎胃散治疗慢性萎缩性胃炎及胃癌前病变的研究

目的：观察萎胃散对慢性萎缩性胃炎（CAG）及肠上皮化生、异型增生的临床疗效并进行实验研究。方法：选择经胃镜加病理检查确诊的CAG患者200例进行分组对照治疗，其中萎胃散治疗组135例，胃复春对照组65例。同时对大鼠CAG模型，分别进行萎胃散治疗与氯化钠溶液灌胃，观察比较胃粘膜固有腺体萎缩程度。结果：CAG萎胃散治疗组总有效率为77.04%，胃复春对照组总有效率为66.15%，两组比较差异有非常显著性意义（P＜0．01）；对肠上皮化生、异型增生也有改善作用，但与对照组比较差异无显著性意义（P＞0．05）。实验研究表明，胃萎散治疗组的CAG病变数量明显减少，病理检查可见腺体恢复正常。结论：胃萎散治疗CAG有明显的效果，对胃癌前病变也有改善作用。     

Bilateral adrenalectomy: effect of tryptophan on protein synthesis and pepsin activity in the stomach of rats.

The effect of bilateral adrenalectomy and subsequent force-feeding of L-tryptophan on the gastric mucosal pepsin activity and [3H]leucine incorporation into total protein of the stomach (fundus) in vivo were investigated. One month after bilateral adrenalectomy the gastric mucosal pepsin activity and overall protein synthesis in the stomach were decreased by 72% and 52%, respectively. Twenty-four hours after a single tube-feeding of tryptophan (30 mg/100 g body weight) both activities returned to sham-operated control levels. In adrenalectomized rats the tryptophan-mediated stimulation of gastric mucosal pepsin activity was found to be sensitive to the RNA synthesis inhibitor, actinomycin-D. The diminution in gastric mucosal pepsin activity after adrenalectomy and its enhancement by tryptophan could not be related to the presence of an inhibitor or activator in the tissue. One month after adrenalectomy serum gastrin concentration was found to be 36% above that of the sham-operated control. In adrenalectomized rats, 24 and 48 h after tryptophan force-feeding, serum gastrin concentrations were decreased by 50% and 20%, respectively, but none of the values differed significantly from those of water-fed adrenalectomized controls.