马来酸伊索拉定对阿司匹林所致大鼠胃黏膜损伤的保护作用

目的探讨马来酸伊索拉定对阿司匹林所致大鼠胃黏膜损伤的保护作用及其机制。方法 60只健康雄性Wistar大鼠随机分成5组:空白对照组、阿司匹林损伤组、马来酸伊索拉定保护组、硫糖铝保护组、奥美拉唑保护组。各保护组分别用马来酸伊索拉定(10 mg/kg)、硫糖铝(600 mg/kg)及奥美拉唑(10 mg/kg)提前给大鼠灌胃,阿司匹林损伤组用生理盐水(9 mg/ml)灌胃,再用阿司匹林(150 mg/kg)灌胃致急性胃黏膜损伤,测量各组胃黏膜溃疡指数(UI)、黏膜损伤积分(EDS)、胃黏膜血流值、一氧化氮(NO)、氨基己糖、白介素-1(IL-1)、肿瘤坏死因子-α(TNF-α)的含量,并在显微镜及电镜下观察胃黏膜组织学改变。结果马来酸伊索拉定保护组各项检测指标显示:UI、EDS明显低于阿司匹林损伤组(P0.01),高于奥美拉唑保护组(P0.05),略低于硫糖铝保护组(P0.05);胃黏膜血流值明显高于阿司匹林损伤组和硫糖铝保护组(P0.05),略低于奥美拉唑保护组(P0.05);NO含量明显高于阿司匹林损伤组(P0.01)和奥美拉唑保护组(P0.05),略低于硫糖铝保护组(P0.05);氨基己糖含量明显高于阿司匹林损伤组(P0.01),低于奥美拉唑保护组(P0.05),略高于硫糖铝保护组(P0.05);IL-1、TNF-α含量明显低于阿司匹林损伤组、奥美拉唑保护组及硫糖铝保护组(P0.01)。结论马来酸伊索拉定可以增加胃黏膜血流、NO及氨基己糖含量,同时抑制炎症性细胞因子IL-1、TNF-α的产生,对阿司匹林所致大鼠急性胃黏膜损伤有明显的预防保护作用。     

瑞巴派特对大鼠急性酒精性胃黏膜损伤的保护作用

目的 探讨瑞巴派特对大鼠急性酒精性胃黏膜损伤的保护作用。方法用酒精或酒精和瑞巴派特直接灌胃的方法制作大鼠急性胃黏膜损伤模型，对比观察不同时点（0、15、30、60min）大鼠胃黏膜的损伤指数；采用免疫组化ABC法测定组织中的TNF-α，采用ELISA法和硝酸还原酶法分别测定血浆PGE，和血清NO。结果随时间的推移，酒精刺激后胃黏膜有高度损伤，但同时应用瑞巴派特不仅能使其损伤程度明显降低（与酒精组或对照组相比，P〈0．05），还可抑制酒精诱导的胃黏膜TNF-α的表达，时间越长这种抑制作用越明显；饮酒30min后，瑞巴派特能明显提高血清NO水平（P〈0.01）和血浆PGE：水平（P〈0．05），60min后，瑞巴派特组血浆PGE，水平甚至超过正常对照组（P〈0．01）。结论 瑞巴派特能够降低胃黏膜组织中的TNF-α表达，显著提高血液中的NO和PGE2水平。     

胃舒散对乙醇诱导大鼠急性胃损伤的保护作用

目的研究胃舒散对乙醇所致急性胃黏膜损伤（AGML）的保护作用。方法采用乙醇灌胃诱导大鼠AGML模型。采用光镜、扫描电镜和透射观察不同剂量胃舒散（3．0、1．5、0．75g／kg）对黏膜组织形态学的保护作用，并同时检测胃黏膜局部血流量（GMBF）、跨膜电位（PD）、胃组织超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量和血浆NO水平，等容积的生理盐水和丽珠得乐（1．0g／kg）分别作为正常对照和治疗对照组。结果胃舒散组胃黏膜损伤指数及组织学评分均较模型对照组显著降低（P〈0．05，P〈0．01）；GMBF及PD较模型对照组显著增高（P〈0．0l，P〈0．05）；胃舒散可明显提高胃组织SOD活性（P〈0．05）及血浆NO水平（P〈0．叭）。结论胃舒散对乙醇所致AGML有明显的保护作用，其作用机制可能与增加胃黏膜血流及抗氧化作用有关。     

长期饮酒胃黏膜病理改变与PGE2和EGF的关系

目的探讨长期饮酒患者胃黏膜病理改变与PGE2和EGF的关系。方法选择因长期饮酒于2007年1月～2010年12月在我院进行胃镜检查并进行胃黏膜活检及血液和胃液前列腺素E2（PGE2）和表皮生长因子（EGF）检测的120例患者作为研究对象。按组织病理学分组进行对照研究。结果与长期饮酒轻度胃黏膜慢性炎症组患者比较,长期饮酒胃黏膜中重度慢性炎症组患者血清和胃液EGF明显升高（P=0.000;P=0.028）,而血清和胃液PGE2升高不明显（P=0.089;P=0.760）。与长期饮酒胃黏膜轻度萎缩组患者比较,长期饮酒胃黏膜中重度萎缩组患者血清EGF明显升高（P=0.000）,而胃液EGF和血清PGE2降低（P=0.846;P=0.362）,胃液PGE2略升高（P=0.936）。与长期饮酒胃黏膜轻度肠化组患者比较,长期饮酒胃黏膜中重度肠化组患者血清EGF明显升高（P=0.000）,而胃液EGF、血清和胃液PGE2升高,但差异无统计学意义（P=0.123;P=0.621;P=0.154）。与长期饮酒胃黏膜无不典型增生组患者比较,长期饮酒胃黏膜不典型增生组患者血清和胃液EGF明显升高（P=0.000;P=0.003）,而血清和胃液PGE2虽升高,但差异无统计学意义（P=0.329;P=0.618）。结论长期饮酒引起EGF分泌升高与胃黏膜慢性炎症、胃黏膜癌前状态和癌前病变的发生和发展有一定的关系,但PGE2在上述病变中变化并不一致,有待于进一步研究。     

荆花胃康胶丸对大鼠胃黏膜的保护机制

目的:研究中药制剂荆花胃康胶丸对大鼠乙醇性急性胃黏膜损伤的预防和治疗作用并探讨其作用机制.方法:将84只SD大鼠随机分为7组,每组12只.Ⅰ组为空白对照组,Ⅱ组为预防组,Ⅲa组为治疗对照组,Ⅲb为达喜对照组,Ⅲc,Ⅲd,Ⅲe分别为荆花胃康胶丸10,20,30 mg/(kg·d)治疗组.于治疗1,3,7 d分别处死大鼠,检测黏膜损伤指数,刮取胃黏膜测定组织中前列腺素E2(PGE2)和表皮生长因子(EGF)的含量,并作组织学观察.结果:荆花胃康胶丸的不同剂量组可不同程度的减轻无水乙醇对大鼠胃黏膜的损伤(P＜0.05,P＜0.01),增加组织中PGE2和EGF的含量(P＜0.05,P＜0.01),效应与剂量及治疗时间成正比.达喜及荆花胃康胶丸治疗组在治疗同一时间段的黏膜炎症程度明显轻于Ⅲa组,黏膜细胞水肿、变性减轻,炎性细胞减少.同时预先给予一定剂量的荆花胃康胶丸与同样浓度的治疗组相比,能明显增加黏膜中PGE2(3 d:190.73±12.20 pg/g vs 158.46±11.44 pg/g;P＜0.05)和EGF(3 d:5.60±0.46 ng/g vs 4.56±0.70 ng/g,P＜0.05)的含量,减轻无水乙醇对大鼠胃黏膜的损伤程度(3 d:10.50±2.08 vs 18.25±1.50,P＜0.05).结论:荆花胃康胶丸对乙醇所致大鼠急性胃父黏膜损伤有预防及修复治疗作用,其作用机制可能与增加胃黏膜中PGE2和EGF有关.     

胃黏膜保护剂的作用及其机制的研究

目的 比较枸橼酸铋钾－1、枸橼酸铋钾－2及蔗糖硫酸酯碱式铝盐（硫糖铝）对胃黏膜的保护作用并研究作用机制。方法 采用乙醇、应激、阿司匹林及盐酸诱发大鼠胃黏膜急性损伤，用50％醋酸接触胃浆膜面产生慢性胃溃疡。枸橼酸铋钾－1、2和硫糖铝的急性损伤药物剂量分别为37.5,40和335mg/kg。给药3d，每天2次；慢性溃疡给药的剂量同急性损伤剂量，但给药11d，每天2次。检查损伤指数及溃疡面积。结果 （1）枸橼酸铋钾－1、枸橼酸铋钾－2和硫糖铝有低抗乙醇、应激、阿司匹林和盐酸诱发的胃黏膜损伤作用，并促进醋酸溃疡的愈合。（2）这种保护黏膜、促进溃疡愈合的作用机制与增加胃黏膜血流量、增加胃黏膜的醌还原酶、谷胱甘肽S－转移酶（GST）和谷胱甘肽还原酶（GR）的 活性及增加碱性成纤维生成因子（bFGF)mRNA和诱导型一氧化氮合酶（iNOS)mRNA的表达有关。结论 保护黏膜药枸橼酸铋钾－1、枸橼酸铋钾－2及硫糖铝有抵抗损伤，促进溃疡愈合的作用，其作用机制是增加胃黏膜血流量，减少氧自由基，增加bFGF及NOS。     

艾灸刺激对腓总神经横断术后大鼠胃黏膜修复作用机制的影响

目的:为探讨艾灸启动内源性保护信息对胃黏膜的保护效应与腓总神经通路的关系.方法:将48只SD大鼠随机分为正常组A组,模型组B组,艾灸模型组C组,艾灸模型手术组D组,每组12只.予C、D组腓总神经切断术,术后护理处理3 d.除A予以生理盐水灌胃外,其余各组用无水乙醇、阿司匹林灌胃制备胃黏膜损伤模型.C组、D组给予艾灸"足三里(ST36)"治疗,2次/d,连续治疗3 d.3 d后观察胃黏膜损伤指数(ulcerindex,UI);胃黏膜相关修复细胞因子,表皮生长因子(epidermal growth factor,EGF)、前列腺素2(prostaglandin E2,PGE2)检测;胃黏膜细胞凋亡指数(apoptosis index,AI)检测.结果:与C组相比,D组在病理切片,UI改变效果较差(P=0.014);血清与组织中胃黏膜细胞相关修复因子E G F、P G E2增加不明显(血清EGF:P=0.003,组织EGF:P=0.000;血清PEG2:P=0.000,组织PGE2:P=0.000);胃黏膜凋亡蛋白AI比例增加不明显(P=0.000).结论:艾灸刺激足三里穴可通过腓总神经途径传递信息,调节胃黏膜保护因子的释放,并调控细胞凋亡相关蛋白表达,从而达到修复胃黏膜的效应.     

复方田七胃痛胶囊对胃溃疡大鼠胃黏膜一氧化氮及内皮素的影响

[目的]通过观察复方田七胃痛胶囊对胃溃疡(GU)大鼠胃黏膜一氧化氮(NO)、一氧化氮合酶(NOS)以及内皮素(ET)水平的影响,探讨其保护胃黏膜损伤的可能机制.[方法]采用Okabe乙酸烧灼法制作大鼠胃前壁溃疡模型,随机将模型动物分为模型组,复方田七胃痛胶囊(简称复方田七)大、中、小剂量组,硫糖铝及法莫替丁组,各组分别连续给药治疗10 d.给药结束后,检测溃疡周围组织NO、NOS及ET的水平.[结果]与模型组相比,所有给药组均能够提高胃组织NO及NOS的水平,减低大鼠胃组织ET的水平(P＜0.01);其中复方田七大剂量组的作用最强.[结论]复方田七胃痛胶囊提高大鼠胃组织NO及NOS、显著降低ET水平,可能是提高大鼠GU黏膜愈合程度的作用机制之一.     

小檗碱对非甾体消炎药相关性肠损伤的保护作用及其机制研究

背景：近年非甾体消炎药（NSAIDs）相关性肠损伤的发生率明显升高,但目前尚缺乏有效防治NSAIDs相关性肠损伤的药物。目的：研究中药小檗碱对NSAIDs相关性肠损伤的治疗作用及其机制。方法：将40只大鼠随机分为对照组、模型组以及低、中、高剂量小檗碱干预组（分别为25、50、75mg·kg-1·d-1）。采用7.5mg·kg-1·d-1双氯芬酸制备NSAIDs相关性肠损伤模型。造模第5d处死所有大鼠,行小肠黏膜大体、组织学评分。以ELISA法检测小肠黏膜前列腺素（PG）E2含量,硝酸还原酶法检测小肠黏膜和血清NO含量,免疫组化法检测小肠黏膜环氧合酶（COX）-1、COX-2表达。结果：与对照组相比,模型组大鼠小肠大体评分和组织学评分明显升高（P〈0．05）,小肠黏膜PGE,含量明显降低（P〈0．05）,小肠黏膜和血清NO含量明显升高（P〈0．05）,小肠黏膜COX-1表达明显降低（P〈0．05）,COX-2表达明显升高（P〈0．05）。给予低、中、高剂量小檗碱干预后,上述指标明显改善（P〈0．05）。结论：小檗碱对NSAIDs相关性肠损伤具有保护作用,其机制可能与小檗碱致小肠黏膜PGE：、COX-1表达升高以及组织和血清NO含量、COX-2表达降低有关。     

艾灸预处理对应激性溃疡大鼠胃黏膜HSP70蛋白及mRNA表达的影响

目的:观察艾灸足三里和梁门穴预处理对应激性溃疡大鼠胃黏膜热休克蛋白70(HSP70)及其基因表达的影响,探讨艾灸足阳明经穴保护胃黏膜的作用机制.方法:将60只大鼠完全随机分为空白组(A)、模型组(B)、艾灸足三里等穴组(C)和对照组(D)4组,采用水浸-束缚应激法(WRS)制备应激性溃疡模型.按Guth法计算胃黏膜损伤指数(UI),用免疫组织化学法、逆转录聚合酶链式反应(RT-PCR)法和放射免疫法分别检测处理后大鼠胃黏膜HSP70,HSP70mRNA的表达和内皮素(ET)、前列腺素E2(PGE2)的含量.结果:SU大鼠胃黏膜损伤指数B组与A、C组(P=0.000,P=0.001),D组与A、C组(P=0.001)有显著性差异,艾灸足三里等穴可使SU大鼠胃黏膜损伤指数明显下降.胃黏膜PGE2含量A组与B、D组比较差异显著(P=0.011,P=0.028),C组与B、D组比较差异显著(P=0.020,P=0.048),经艾灸预处理的大鼠胃黏膜PGE2含量均有不同程度升高.ET含量B组与A组之间有显著差异(P=0.040),经艾灸预处理的大鼠ET含量下降显著,B组与C组相比差异显著(P=0.020).造模后胃黏膜的HSP70蛋白和mRNA表达均有不同程度的增强,B组与A组相比有显著性差异(P=0.039,P=0.008);经艾灸预处理后HSP70蛋白和mRNA显著增强,C组与B、D组比较有统计学意义(蛋白:P=0.003,P=0.035;mRNA:P=0.000,P=0.001).结论:艾灸足三里、梁门穴能通过增强HSP70的蛋白和基因表达,达到对胃黏膜的保护作用,并有一定的穴位特异性.     

Effects of propranolol and sucralfate on ethanol-induced gastric mucosal damage in chronic portal hypertensive rats

In a rat model of chronic portal hypertension we studied ethanol-induced gastric mucosal damage and the effects of pretreatment by propranolol and sucralfate. Susceptibility to ethanol was increased in chronic portal hypertensive rats compared with sham-operated rats (55 +/- 8% vs. 25 +/- 4%). Both acute pretreatment (10 min) and chronic pretreatment (3 weeks) with propranolol reduced gastric mucosal injury induced by ethanol in portal hypertensive rats, compared with saline-treated rats. Acute and chronic pretreatment with propranolol had no protective effect in sham-operated rats. In portal hypertensive rats, sucralfate in two different doses (500 and 125 mg/kg) protected the gastric mucosa against ethanol-induced gastric injury compared with animals receiving saline (2 +/- 1% and 3 +/- 2% vs. 25 +/- 3%). Sucralfate at the higher dose did not reduce portal pressure in portal hypertensive rats. We conclude that: (1) chronic portal hypertension increases ethanol-induced gastric damage; (2) acute and chronic propranolol treatment reduces ethanol-induced gastric injury in portal hypertensive rats, probably by decreasing portal hypertension; (3) sucralfate has a cytoprotective effect in portal hypertensive rats without reducing portal pressure. These results suggest a potential application of sucralfate in patients otherwise treated by sclerotherapy.     

Effect of intragastric pH on mucosal protective action of sucralfate.

Acid intragastric pH is believed to be mandatory for mucosal protective action of sucralfate, but evidence for its efficacy at neutral pH is lacking. The effect of sucralfate on gastric mucosal erosions induced by oral administration of aspirin and bile acids at acidic pH of 1.5 and 3.9, and near neutral pH of 6.5 was investigated in 320 rats. The effect of sucralfate on the intragastric pH four hours after the ingestion of test solutions was also examined. The incidence and severity of mucosal erosions induced by aspirin and bile acids were lower in animals treated with sucralfate at acidic (p less than 0.001) and near neutral (p less than 0.01) intragastric pH. Mucosal protection was greater with ingestion of sucralfate 300 mg/kg and 200 mg/kg, than with 100 mg/kg. The intragastric pH was higher (p less than 0.001) in sucralfate treated groups at pH 3.9 and 6.5. This study provides evidence that sucralfate protects against mucosal injury at near neutral, as well as at acidic pH.     

The effect of misoprostol, omeprazole and sucralfate on nicotine- and ethanol-induced gastric injury and gastric mucosal blood flow: A comparative study

Nicotine, which is thought to be responsible for part of the pharmacological effect of smoking, exacerbates gastric mucosal injury in rats. The effects of misoprostol (12.5 micrograms to 100 micrograms), omeprazole (12.5 mg to 100 mg) and sucralfate (50 to 400 mg) on gastric mucosal blood flow and mucosal injury induced by nicotine were studied in an ex vivo gastric chamber preparation in rats. Rats were pretreated with nicotine (25 micrograms/mL orally) for 10 days and ethanol was added to the gastric chamber preparation. Laser Doppler flowmetry was used to measure the gastric mucosal blood flow and mucosal damage (ulcer index) was assessed by the area of haemorrhagic lesions. The ulcer index was significantly higher in rats pretreated with nicotine. Treatment with misoprostol and omeprazole lowered the ulcer index significantly compared with controls. The peak and summation blood flows were lower in nicotine-treated rats but failed to reach statistical significance. The peak blood flow (blood flow at 45 min) and the summation blood flow were significantly higher with all doses of sucralfate, misoprostol and omeprazole than in controls (P less than 0.05). The increase in gastric mucosal blood flow was significantly higher with sucralfate and misoprostol than with omeprazole. We conclude that sucralfate, misoprostol and omeprazole prevent nicotine- and ethanol-induced gastric mucosal damage and are accompanied by an increase in gastric mucosal blood flow. This indicates that smoking exacerbates gastric mucosal injury and that cytoprotective and site-protective agents can reduce injury by these noxious agents.     

Effect of sucralfate on gastric mucosal blood flow in rats.

Sucralfate possesses site protective and cytoprotective actions and heals ulcers effectively, but its effect on gastric mucosal blood flow is unknown. Using an ex vivo gastric chamber preparation, we studied the effect of sucralfate on gastric mucosal blood flow in rats by laser doppler flowmetry. Under both fasting and fed states, measurements of gastric mucosal blood flow and damage were made in rats after topical application of absolute ethanol alone or after pretreatment with sucralfate. Gastric mucosal damage was assessed by measuring the total area of haemorrhagic mucosal lesions. Ethanol induced gastric mucosal lesions were significantly less with sucralfate pretreatment than without (p less than 0.008). Mucosal blood flow significantly fell after ethanol application (p less than 0.001). The fall was significantly less in fed than in fasted rats (p less than 0.05), and after pretreatment with sucralfate 100 mg or 200 mg than without in both fasted (p less than 0.0008 and 0.00001, respectively) and fed (p less than 0.002 and 0.001, respectively) rats. Graded doses of sucralfate (25-400 mg) resulted in an increase in gastric mucosal blood flow in a dose dependent manner (r = 0.731, p less than 0.001). In conclusion that sucralfate increases gastric mucosal blood flow in rats and lessens the fall in blood flow in rats treated with ethanol, and this action may contribute to its protection against the vascular damage of mucosa by ethanol.     

Double blind controlled study on the effect of sucralfate on gastric prostaglandin formation and microbleeding in normal and aspirin treated man.

Two groups A and B each comprising 12 healthy young male subjects were used in a double blind, placebo controlled trial to assess the effects of 1.0 g sucralfate qid on prostaglandin (PG) generation and mucosal integrity in the intact and aspirin-treated stomach. Mucosal formation and luminal release of PGE2, 6-keto-PGE1 alpha and thromboxane B2, gastric microbleeding and DNA loss (integrity indicators) and basal and pentagastrin induced acid secretion were measured after placebo and sucralfate treatment in subjects without (group A) and with administration of 2.5 g aspirin (group B). Sucralfate significantly reduced spontaneous gastric microbleeding and DNA loss in group A and prevented blood loss but not DNA loss caused by aspirin in group B. The protective effects of sucralfate on spontaneous gastric microbleeding were accompanied by increased mucosal biosynthesis and luminal release of PGE2 and 6-keto-PGF1 alpha with a reduction in release of thromboxane B2. In aspirin treated subjects both mucosal generation and luminal release of prostaglandins and thromboxane B2 were greatly suppressed although sucralfate treatment did not influence these prostaglandins in spite of the reduction in mucosal damage. It is concluded that sucralfate has a potent protective action on spontaneous and aspirin treated gastric microbleeding in man and that this protection may be partly because of the increased mucosal biosynthesis of prostaglandins.     

巯基物质对小剂量阿司匹林所致大鼠胃黏膜损伤的保护作用

背景：很多胃黏膜损伤模型中发现巯基物质含量下降，巯基物质对胃黏膜细胞具有保护作用。目的：探讨巯基物质对小剂量阿司匹林所致胃黏膜损伤的保护作用。方法：80只雄性Sprague-Dawley（SD）大鼠随机分为正常对照组、纯巯基对照组、阿司匹林模型组、巯基预防组、硫糖铝预防组、NaCl治疗对照组、巯基治疗组和硫糖铝治疗组8组。测定黏膜溃疡指数（UI），行大体、组织学和透射电子显微镜观察，测定胃黏膜组织中还原型谷胱甘肽（GSH）、超氧化物歧化酶（SOD）、丙二醛（MDA）、6-酮．前列腺素F1α（6-keto-PGF1α）水平。结果：阿司匹林模型组胃黏膜发生病变，UI与其余各组相比显著升高（P〈0．01），GSH、6-keto-PGF1α含量较正常对照组显著降低（P〈0．05），MDA含量显著增高（P〈0.001）。巯基预防或治疗后，胃黏膜损伤明显减轻，UI显著下降（P〈0．001），GSH、6．keto．PGF1α含量显著增高（P〈0．05），MDA含量显著降低（P〈0．05）。各组SOD含量无显著差异。结论：小剂量阿司匹林可致大鼠胃黏膜损伤，胃黏膜GSH下降可能是其机制之一。外源性GSH具有增强胃黏膜抗氧化作用和细胞保护作用。     

黏膜保护剂对实验性胃黏膜损伤及胃黏膜超微结构改变的作用

目的 评价铝碳酸镁等常用黏膜保护剂对乙醇、阿司匹林、盐酸、泼尼松龙诱发的大鼠胃黏膜损伤的保护作用,并观察铝碳酸镁的黏膜保护作用与胃黏膜上皮细胞间隙变化的关系.方法 采用四种方法造模.①乙醇造模:采用雄性Wistar大鼠84只,分为7组,每组12只,分别给予铝碳酸镁、麦滋林、替普瑞酮、吉法酯、硫糖铝、瑞巴派特、0.9%氯化钠溶液3 d,第4天动物在给药后再经口给予无水乙醇l ml造模.之后处死动物观察药物对大鼠胃黏膜损伤的作用.计算各组胃黏膜损伤长度(mm)作为损伤指数.②阿司匹林造模:经口给予阿司匹林(300 mg/kg)及0.1 mol/L盐酸0.5 ml/100 g造模,余实验方法同①.③盐酸造模:经口给予0.7 mol/L盐酸1 ml造模,余实验方法同①.④泼尼松龙造模:动物分组及给药剂量同其他模型,给药或0.9%氯化钠溶液5 d,第2～5天每天皮下注射泼尼松龙(250 mg/kg),第5天处死动物,用Guth法计算损伤指数.取每种动物模型对照组及铝碳酸镁组的第1、5和10号动物胃黏膜组织,用透射电镜检测细胞间隙的变化.结果 四种胃黏膜损伤模型中,各黏膜保护剂用药组胃黏膜损伤指数均显著小于对照组(P值均＜0.05),其中铝碳酸镁组与对照组比较差异有统计学意义(P＜0.01).同时铝碳酸镁组胃黏膜上皮细胞间隙显著小于对照组(P＜0.05).结论 六种常用黏膜保护剂对乙醇、盐酸、阿司匹林、泼尼松龙诱发的胃黏膜损伤均有保护作用,其中铝碳酸镁的保护作用更显著.观察胃黏膜上皮细胞间隙可从细胞学水平进一步证实铝碳酸镁的黏膜保护作用.     

莫沙必利对阿司匹林致大鼠急性胃黏膜损伤的保护作用

研究显示促胃肠动力药物莫沙必利对胃黏膜损伤具有一定的保护作用。目的：研究不同剂量莫沙必利对阿司匹林致大鼠急性胃黏膜损伤的保护作用及其机制。方法：将50只大鼠随机分为阴性对照组、单纯损伤组以及不同剂量莫沙必利干预组（0．25mg／kg、0．50mg／kg、0．75mg／kg）。干预组大鼠以不同剂量莫沙必利灌胃行预处理,以150mg／kg阿司匹林灌胃制备急性胃黏膜损伤模型。实验第4d,处死大鼠。评估大鼠胃黏膜损伤指数和组织学变化,以免疫组化法检测Occludin蛋白分布,蛋白质印迹法检测Occludin、ZO．1以及磷酸化ERK（p-ERK）、磷酸化JNK（p-JNK）和磷酸化p38（p-p38）蛋白表达。结果：与单纯损伤组相比,各莫沙必利干预组胃黏膜损伤指数均明显降低（P〈0．05）;胃黏膜组织学明显改善;胃黏膜Occludin、ZO-1蛋白表达呈剂量依赖性升高（P〈0．05）;胃黏膜p-ERK、p-p38蛋白表达呈剂量依赖性降低（P〈0．05）;而胃黏膜p-JNK蛋白表达无明显差异。结论：莫沙必利对阿司匹林致大鼠急性胃黏膜损伤具有明显保护作用,其机制可能为降低MAPKs信号通路中ERK和p38蛋白磷酸化程度,并上调胃黏膜紧密连接蛋白Occludin和ZO-1表达,从而改善胃黏膜屏障的功能。     

Does sucralfate reduce acetylsalicylic-acid-induced gastric mucosal bleeding?

We studied the possible protection of sucralfate with regard to acetylsalicylic acid (ASA)-induced gastric mucosal bleeding as measured by a radiochromium assay of faecal blood loss in a double-blind crossover study involving 16 healthy male volunteers. Medication was given in two combinations during the 2nd and 5th week of the study: 1 g ASA and 1 g sucralfate four times daily, or 1 g ASA four times daily and placebo tablets. Mean faecal blood loss (+/- SEM) was 0.38 +/- 0.04 ml/day in the 1st week (no drugs administered), 7.17 +/- 1.60 ml/day during treatment with ASA + sucralfate, and 9.59 +/- 1.76 ml/day during treatment with ASA + placebo, the difference being not statistically significant. Individual bleeding values registered during sucralfate treatment correlated with those measured in the placebo period. However, three persons with pronounced bleeding after ASA + placebo had minimal bleeding after ASA + sucralfate. Sucralfate may have a protective potential by reducing ASA-induced gastric mucosal bleeding, but further studies are required to evaluate its protective mechanisms and to identify the groups of patients that could benefit from this.