丁桂软胶囊抗实验性胃溃疡的研究

观察丁桂软胶囊抗实验性胃溃疡的药理作用,为其临床应用提供实验依据。方法:采用3种大鼠溃疡模型(乙醇致胃粘膜损伤性胃溃疡、幽门结扎型胃溃疡、应激性胃溃疡)及小鼠利血平胃溃疡模型,以溃疡指数、溃疡抑制百分率、溃疡面积及溃疡发生     

半胱氨酸对大鼠浸水应激性胃溃疡的影响

目的；研究半胱氨酸对大鼠胃溃疡的影响及其作用机制，方法：利用大鼠浸水应激性胃溃疡模型，观察腹注盐酸半胱氨酸对胃溃疡指数、胃粘膜谷胱甘肽（ＧＳＨ）含量１胃酸分泌和胃粘液分泌的影响。结果：半胱氨酸能抑制大鼠胃溃疡的形成；浸水应激可使大鼠胃粘膜ＧＳＨ含量明显降低，半胱氨酸对ＧＳＨ含量的降低无影响；事先给予Ｎ－乙酰马来酰氨或消炎痛对半胱氨酸的抗溃疡作用无影响；半胱氨酸能抑制浸水应激大鼠胃酸的分泌，但对胃粘     

Effect of cysteine on gastric mucosal lesion induced by restraint water-immersion in rats

目的：研究半胱氨酸对大鼠胃溃疡的影响及其作用机制。方法：利用大鼠浸水应激性胃溃疡模型，观察腹注盐酸半胱氨酸对胃溃疡指数、胃粘膜谷胱甘肽（ＧＳＨ）含量、胃酸分泌和胃粘液分泌的影响。结果：半胱氨酸能抑制大鼠胃溃疡的形成；浸水应激可使大鼠胃粘膜ＧＳＨ含量明显降低，半胱氨酸对ＧＳＨ含量的降低无影响；事先给予Ｎ－乙酰马来酰氨（Ｎ－ｅｔｈｙｌｍａｌｅｉｍｉｄｅ，ＮＥＭ）或消炎痛对半胱氨酸的抗溃疡作用无影响；半胱氨酸能抑制浸水应激大鼠胃酸的分泌，但对胃粘液的分泌无影响。结论：半胱氨酸的抗溃疡作用与其抑制胃酸分泌有关，而与胃粘液的分泌、胃粘膜ＧＳＨ和前列腺素的作用无关。     

大鼠侧脑室注射GABA对束缚-浸水应激性胃溃疡的影响

为探索脑内γ-氨基丁酸(GABA)对应激性胃溃疡的影响及其机制,采用大鼠束缚-浸水应激性胃溃疡模型,观察了侧脑室注射γ-氨基丁酸及其A型受体的激动剂和拮抗剂对大鼠应激性胃溃疡的影响。结果表明:与侧脑室注射生理盐水组比较:(1)侧脑室注射γ-氨基丁酸,大鼠束缚-浸水应激性胃溃疡程度显著减轻(P<0.01);(2)侧脑室注射戊巴比妥钠(GABAA型受体激动剂),胃溃疡程度也显著减轻(P<0.05);(3)侧脑室注射荷包牡丹碱(GABAA型受体拮抗剂),胃溃疡程度明显加重(P<0.05)。这些结果表明:外源性γ-氨基丁酸对大鼠束缚-浸水应激性胃溃疡的形成有抑制作用,这种抑制作用是通过脑内GABAA型受体介导的;在应激过程中,脑内也有内源性γ-氨基丁酸的释放并通过其A型受体的活动,减轻胃溃疡的形成。     

十五味黑药丸对大鼠应激性胃溃疡的影响

目的:观察十五味黑药丸对大鼠应激性胃溃疡的治疗效果。方法:SD大鼠分为五组,即十五味黑药丸0.5 g.kg-1、1.0 g.kg-12、.0 g.kg-1剂量组,甲氰咪胍阳性对照组(0.1 g.kg-1),阴性对照组(生理盐水);各组连续给药7天,末次给药后水浴法造成大鼠应激性溃疡,20小时后放血处死动物;检查胃病变情况,由此观察十五味黑药丸对溃疡的治疗作用。结果:十五味黑药丸组大鼠溃疡面积和溃疡指数均明显小于对照组,其中以2.0 g.kg-1组作用最为显著(P<0.01)。结论:十五味黑药丸对大鼠应激性胃溃疡具有明显的防治作用。     

三种不同药物治疗胃溃疡的临床效果分析

目的探讨三种不同药物(奥美拉唑、兰索拉唑和泮托拉唑)治疗胃溃疡的临床效果分析。方法选取我院收治的102例胃溃疡患者作为研究对象,随机分为奥美拉唑组(采用奥美拉唑治疗)、兰索拉唑组(采用兰索拉唑治疗)和泮托拉唑(采用泮托拉唑治疗)组,每组各34例。治疗结束后比较三组患者的临床疗效和不良反应发生情况。结果泮托拉唑组、兰索拉唑组、奥美拉唑组患者的临床总有效率分别为91.18%(31/34)、82.35%(28/34)、85.29%(29/34),三组患者临床总有效率比较,差异无统计学意义(P0.05);泮托拉唑组、兰索拉唑组、奥美拉唑组患者的不良反应发生率分别为2.94%(1/34)、20.59%(7/34)、17.65%(6/34),泮托拉唑组患者不良反应发生率明显低于兰索拉唑组和奥美拉唑组,差异具有统计学意义(P0.05)。结论奥美拉唑、兰索拉唑和泮托拉唑抑酸治疗胃溃疡患者临床疗效无明显差异,但常规西医治疗基础上采用泮托拉唑治疗胃溃疡患者不良反应发生率较低,安全性高,有较高的临床应用价值,值得临床推广。     

神经降压素在大鼠应激性胃溃疡中的作用

选健康雄性Ｗｉｓｔａｒ大鼠１２２只，用脑室微量注射和放射免疫等分析方法，观察了中枢内、外源性神经降压素（ＮＴ）在大鼠束缚加水浸诱导的应激性胃溃疡中的作用。结果表明：（１）在大鼠应激性胃溃疡产生的同时，其血浆内神经降压素样免疫活性物（ＮＴＬＩ）的含量明显减少（Ｐ〈０．０５），而下丘脑、中脑、脑桥、延脑和垂体中ＮＴ－ＩＲ含量则明显升高（Ｐ〈０．０１）；（２）侧脑室注射抗ＮＴ血清中，大鼠应激性胃溃疡的产     

花生油灌胃对大鼠浸水应激性胃溃疡和胃运动的影响

采用束缚－浸水应激法建立大鼠应激性胃溃疡模型,观察花生油对胃粘膜损伤程度和胃运动的影响。结果表明,花生油可以明显减轻胃粘膜损伤,明显抑制胃运动,但对胃粘膜血流量无影响。提示抑制胃运动可能是花生油保护大鼠浸水应激性胃粘膜膜损伤的机制之一。     

雷贝拉唑、兰索拉唑及奥美拉唑联合治疗幽门螺旋杆菌感染胃溃疡患者的临床价值分析

目的探讨雷贝拉唑、兰索拉唑及奥美拉唑联合治疗幽门螺旋杆菌感染胃溃疡患者的临床价值。方法选取2017年1月至2019年1月于我院就诊治疗的78例幽门螺旋杆菌感染胃溃疡患者作为研究对象,按照其治疗方法不同将其分为对照组(30例)和观察组(48例)。对照组患者予以雷贝拉唑、兰索拉唑联合阿莫西林等对症治疗,观察组患者予以雷贝拉唑、兰索拉唑联合奥美拉唑进行治疗。治疗结束后比较两组患者的治疗效果。结果观察组患者临床有效率为(100.00%),显著高于对照组(73.33%),差异具有统计学意义(P0.05);治疗后两组患者溃疡面积均较治疗前明显减小,且观察组患者溃疡面积减小程度显著大于对照组(P0.05);治疗后观察组患者幽门螺旋杆菌清除率显著高于对照组(P0.05);对照组和观察组不良反应发生率(13.33%vs 10.42%)比较,差异无统计学意义(P0.05),且两组均未出现延误患者治疗的严重不良后果。结论雷贝拉唑、兰索拉唑及奥美拉唑联合治疗幽门螺旋杆菌感染胃溃疡患者临床有效率和幽门螺旋杆菌清除率均显著提高,有效减小溃疡面积,具有较高的安全性,值得临床推广使用。     

提高激素性股骨头坏死模型成活率的方法

背景：激素性股骨头坏死动物模型建立过程中动物的死亡成为影响实验结果的主要因素。 目的：观察以脂多糖和地塞米松建立股骨头坏死模型,提高模型成功率的方法。 方法：新西兰大白兔48只随机等分为模型组、庆大霉素组、庆大霉素+兰索拉唑组和对照组,前3组连续2 d经耳缘静脉注射脂多糖,再连续3 d,臀部肌肉注射地塞米松注射液建立股骨头坏死模型,庆大霉素组和庆大霉素+兰索拉唑组在建模成功后连续7 d以庆大霉素灌胃,同时庆大霉素+兰索拉唑组肌肉注射兰索拉唑注射液。对照组兔仅注射生理盐水。 结果与结论：模型组、庆大霉素组和庆大霉素+兰索拉唑组均造模成功;其中庆大霉素+兰索拉唑组存活状况最好,3组动物死亡率分别是33.3%,25%,8.3%,模型组、庆大霉素组、庆大霉素组+兰索拉组和对照组兔的死亡数量差异有显著性意义(P < 0.05)。提示在兔激素性股骨头坏死模型建立中,庆大霉素+兰索拉唑的使用,可以提高实验动物的生存率。 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程全文链接：     

花生油灌胃对大鼠浸水应激性胃溃疡和胃运动的影响

采用束缚-浸水应激法建立大鼠应激性胃溃疡模型,观察花生油对胃粘膜损伤程度和胃运动的影响.结果表明,花生油可以明显减轻胃粘膜损伤,明显抑制胃运动,但对胃粘膜血流量无影响.提示抑制胃运动可能是花生油保护大鼠浸水应激性胃粘膜损伤的机制之一.     

硝普钠对大鼠应激性胃粘膜损伤的保护作用

采用浸水束缚应激法建立大鼠应激性胃溃疡模型，观察一氧化氮供体硝普钠对大鼠胃粘膜损伤的保护作用。结果表明，硝普钠可以明显减轻浸水应激引起的胃粘膜损伤，抑制胃运动亢进，同时增加胃粘膜血流量以及血浆和胃粘膜中NO和SOD含量，降低MDA和ET含量。提示硝普钠对浸水应激性胃粘膜损伤的保护作用可能是通过增加胃粘膜血流量和抑制胃运动亢进共同实现的。     

Methimazole prevents stress and chemical induced gastropathy in rats

This investigation was undertaken to study the effect of methimazole (MMI) on gastric acid secretion and stress and chemically induced gastric ulcer in rats. Acid secretion studies were undertaken using pylorus-ligated rats pretreated with MMI (10-100 mg/kg, i.p.). The effect of orally administered MMI on water-immersion restraint (WIR) stress, indomethacin and ethanol-induced gastric ulcers was also tested. The level of myeloperoxidase (MPO), non-protein sulfhydryls (NP-SH) and gastric wall mucus was measured in the glandular stomach of rats following ethanol-induced gastric lesions. There was a dose-dependent inhibition of gastric acid secretion and ulcerogen induced gastric lesion formation in the MMI treated rats. Our morphological and histological studies showed a complete prevention of ethanol-induced lesions in the rats treated with high dose (100 mg/kg) of MMI. A significant attenuation of ethanol-induced increase in gastric MPO activity, depletion of NP-SH and reduction of gastric wall mucus was also observed in MMI treated rats. These findings clearly suggest the involvement of endogenous pro-inflammatory agents and oxidative stress in mediating the gastroprotective effect of MMI.     

Changes in mucosal superoxide dismutase activities of gastric lesions

The mucosal superoxide dismutase (SOD) activities were serially examined on the acute gastric mucosal lesion (AGML) induced by water-immersion restraint stress to rats for six hours. The mucosal SOD activities gradually increased in proportion to the time up to 3 hours after the restraint stress. But it decreased 6 hours after when severe damage had been established in the mucosa. On the other hand, the mucosal SOD activities of the margins of human gastric ulcer showed to be higher on the healing stage than on the active stage. And the SOD activities of the intractable ulcer were lower than those of the curable ulcer. These results indicate that the mucosal SOD may play some important roles both on the protecting process information of AGML and on the healing process in gastric ulcer.     

Histo-chemical studies on the anti-ulcer effect of bamboo grass in rats

Oral administration of a hot-water extract (Folin) of bamboo grass (Sasa albomarginata Makino & Shibata) significantly reduced the incidence of water-immersion and restraint stress-, ethanol-induced and indomethacin-induced gastric ulcers in rats. Histological examination of the Folin-treated gastric mucosa showed that microscopic blood clots overlaid the superficial epithelium, maintaining the cellular integrity of gastric mucosa, especially against stress ulcer. In addition, Folin suppressed the incidence of hyperaemia and a decline of acid mucopolysaccharides in the ethanol-induced ulcer. Folin suppressed a release of histamine from rat mast cells, and stabilized erythrocytes and accelerated their agglutination under acid conditions. These results suggest that a microscopic haemostatic effect of Folin reinforced by a membrane-stabilizing effect might be responsible for the prevention of the gastric lesions.     

On the possible role of different endogenous opiate receptors in gastroduodenal ulceration of the rat

In Wistar rats of both sexes stress(restraint)- and drug (indomethacin)-induced gastric, as well, as cysteamine-induced duodenal ulceration was treated by morphine and nalorphine, given either alone or in combination.Neither morphine nor nalorphine had a significant anti-ulcerogenic effect. In contrast, the combined morphine+nalorphine treatment showed a highly significant anti-ulcerogenic action in the case of gastric ulceration but it was ineffective on duodenal ulcer formation. It seems that the and endogenous opiate receptors play a significant role in the anti-ulcerogenic effect, while the receptors are involved to a considerably lesser degree.Moreover, the experimental results strengthen the view that gastric and duodenal ulceration are two different pathological entities and that ulcer formation is only a common consequence.     

Gastric healing effect of melatonin against different gastroinvasive agents in cholestatic rats

Background and objective: The frequency of gastrointestinal ulceration is higher in jaundiced patients than in healthy population. The aim of this study was to assess the effect of pretreatment with melatonin, a potent scavenger of reactive oxygen species, on stress-induced gastric ulcers of cholestatic rats. Materials and methods: Cholestasis was induced by surgical ligation of bile-duct and sham-operated rats served as sham animals. The animals received saline or melatonin (1, 3 or 10 mg/kg) before stress induction. Three different types of gastroinvasive agents including ethanol, indomethacin or water immersion were used as stress agents to induce gastric ulceration. Results: Gastric mucosal damage induced by different gastroinvasive agents was significantly greater in bile-duct-ligated rats than in sham ones. Melatonin was protective against ethanol-, indomethacin- and water immersion-induced gastric damage in bile-duct-ligated and sham rats, dose-dependently, but the protective effect of melatonin was greater in cholestatic rats than sham rats in all three different series of experiments. Conclusions: In conclusion, pretreatment of rats with melatonin protected gastric mucosa of cholestatic rats more effectively than the sham ones possibly by a mechanism involving the scavenging of free radicals.     

The effect of exercise training on restraint ulcers in rats

The effect of chronic treadmill running on susceptibility to restraint-cold-induced ulcers was studied in two strains of rats: Long-Evans and Sprague-Dawley. Runners were progressively trained for 8 weeks, reaching a rate of 1 mph for 1 hr daily, 5 days per week after the 4th week. Walkers were exposed to the treadmill environment 3 days per week (0.2 mph for 10 min). Sedentary groups remained in their home cages. After 8 weeks the rats were starved for 24 hrs, immobilized in restraint cages and placed in the refrigerator (5° C) for 4 hrs. Animals were then sacrificed and their stomachs examined for ulcerative lesions. No significant differences in number of ulcers or ulcer indexes per stomach were found between groups within each rat strain or between strains. These results suggest that treadmill running provides no protection against gastric ulceration induced by restraint-cold stress. The complex variables involved in ulcer research are discussed and suggestions presented for future work on the anti-ulcer effect of exercise.Supported in part by the University of Nebraska Research Council Summer Fellowship.     

束缚应激对大鼠血小板-氧化氮释放的影响

目的 观察急性应激对大鼠血小板一氧化氮(NO)释放的影响及其机制.方法 大鼠浸水-束缚应激(WRS)2、4和8 h,以胃溃疡指数(UI)作为应激损伤的标识,采用Greiss法测定血小板孵育液中亚硝酸盐(NO2-)含量;同位素法测其一氧化氮合酶(NOS)活性和L精氨酸(L-Arg)转运量.结果 WRS 2 h血小板L-Arg转运量、NOS活性和孵育液NO2-含量较对照组显著增加,但随应激时间延长,其呈下降趋势,应激8 h时均显著低于对照组,胃溃疡逐渐加重.结论 WRS应激早期阶段可上调血小板L-Arg/NO通路,促进血小板NO生成;长时间应激下调L-Arg/NO通路,减少NO释放.     

银杏内酯A对应激性溃疡发生的抑制作用

目的:探讨银杏内酯A (Ginkgolide A) 对大鼠应激性溃疡发生的抑制作用及其可能机制。 方法:Wistar大鼠,随机分成对照组和银杏内酯预处理组;以束缚水浸法建立应激性溃疡模型,通过胃窦部埋置电极记录应激状态下胃平滑肌自发电活动的变化,并测定血浆MDA 含量和SOD活性以及观察胃粘膜的病理学改变。 结果:银杏内酯A 5~20 mg/kg 腹腔注射预处理组,应激所致的胃肌电活动紊乱和血浆MDA 水平以及胃粘膜溃疡指数均明显低于对照组(P＜ 0.05);而血浆SOD活性则高于对照(P＜0.01),其效应具有剂量依赖性。结论:血小板活化因子拮抗剂银杏内酯A 能明显减轻束缚水浸应激引起的大鼠胃粘膜溃疡的发生,其机制可能是通过减少自由基产生和增加其清除,改善胃平滑肌动力障碍。