胃散对胃溃疡模型大鼠胃黏膜保护作用的研究

目的 研究胃散对胃溃疡大鼠胃黏膜的保护作用。方法 采用乙酸烧灼型胃溃疡模型、幽门结扎型胃溃疡模型、乙醇损伤型胃溃疡模型,检测溃疡指数、胃酸总酸度、胃酸分泌速度和胃蛋白酶活性,综合考察胃散对胃溃疡模型大鼠胃黏膜的保护作用。结果 胃散在1、0.5、0.25 g/kg剂量下,对乙酸烧灼型胃溃疡有非常显著的促愈合作用;对幽门结扎型胃溃疡的形成有显著的抑制作用;对乙醇损伤的胃黏膜也有显著的保护作用;对胃液总酸度、胃酸分泌速度和胃蛋白酶活性有明显抑制作用,显著增加胃液分泌量。结论 胃散具有增加胃液分泌、抑制胃酸分泌、抑制胃蛋白酶活性、保护胃黏膜和防止胃溃疡的作用。     

栀子总苷对幽门结扎大鼠胃溃疡保护作用的实验研究

目的：研究栀子总苷（TGZ）对幽门结扎模型大鼠胃溃疡的影响,初步探讨其抗溃疡作用的机制。方法：采用大鼠幽门结扎的方法建立大鼠胃溃疡模型,收集胃液测定胃液游离酸和总酸、胃蛋白酶活性以及观察胃黏膜损伤指数。结果：TGZ灌胃70或140mg/kg5d能显著抑制幽门结扎大鼠胃溃疡的发生,抑制胃液量,降低胃液中游离酸度与总酸度,有效降低胃液中胃蛋白酶活性。结论：栀子总苷对幽门结扎所致的大鼠胃溃疡具有明显的保护作用,与其抑制胃酸分泌和胃蛋白酶的活性有关。     

石榴皮提取物对大鼠幽门结扎所致胃损伤的保护作用研究

目的:研究石榴皮提取物对大鼠实验性胃损伤的保护作用及其与胃黏膜前列腺素E(2PGE2)和6-酮-前列腺素F1α(6-keto-PGF1α)的关系。方法:采取大鼠幽门结扎型胃溃疡模型,观察石榴皮提取物灌胃对实验性胃损伤黏膜的影响,对胃液量、总酸度、游离酸度、总酸排出量和胃黏液、胃蛋白酶分泌的影响;采取放射免疫方法研究对大鼠胃黏膜PGE2和6-keto-PGF1α含量的影响。结果:石榴皮提取物(150、500mg·kg-1)灌胃,可显著抑制大鼠幽门结扎型胃溃疡的形成,促进胃黏液的分泌(P<0.05),但对胃液量、总酸度、游离酸度、总排酸量和胃蛋白酶活性无显著性影响;PGE2和6-keto-PGF1α的含量均增高,其中PGE2含量显著增加(P<0.05)。结论:石榴皮提取物对大鼠幽门结扎所致胃损伤具有良好的保护作用,这种作用可能与促进胃黏液分泌和增加PG合成有关。     

六叶能消胶囊抗大鼠胃溃疡的研究

目的 研究六味能消胶囊对幽门结扎型大鼠胃溃疡模型的影响及其作用机制.方法 采用幽门结扎法制备大鼠胃溃疡模型,观察溃疡指数.测其胃液量、胃液总酸度、胃蛋白酶活性;制备胃组织匀浆,测其一氧化氮(NO)、丙二醛(MDA)的含量及超氧化物歧化酶(SOD)的活性.结果 六味能消胶囊对幽门结扎型胃溃疡大鼠的溃疡、胃液量、总酸度及胃蛋白酶活性均有明显的抑制作用,能显著增加胃组织中NO含量和SOD活性,降低MDA的含量.结论 六味能消胶囊具有一定的抗胃溃疡作用.     

壳聚糖对大鼠胃损伤时黏膜的保护作用

目的研究壳聚糖对大鼠急性损伤时胃黏膜的保护作用。方法采用幽门结扎法建立大鼠损伤模型,然后收集胃液、胃损伤指数计分及SP免疫组化法实验。结果与对照组比较,实验组黏膜损伤指数显著下降(P<0.001);胃内游离酸和总酸度显著降低(P<0.05);诱导型一氧化氮合酶(iNOS)表达显著升高(P<0.01)。结论壳聚糖处理可明显减轻大鼠幽门结扎所致的胃黏膜损伤,对胃黏膜具有很好的保护作用。     

姜油对胃溃疡模型大鼠的影响

［摘要］目的观察姜油对实验性胃溃疡的作用。方法采用大鼠水浸束缚应激致胃溃疡模型、无水乙醇致胃损伤模型和幽门结扎致胃溃疡模型研究不同剂量（50,100,200 mg&#8226;kg 1）姜油对大鼠胃溃疡的预防作用,及对胃液、胃酸分泌、胃蛋白酶活性的影响。结果与模型对照组比较,姜油各剂量组对水浸束缚应激性胃黏膜损伤、无水乙醇致胃黏膜损伤均有良好的保护作用,可使大鼠的溃疡指数显著降低;对幽门结扎型大鼠胃液量、胃酸浓度、胃蛋白酶活性及胃黏膜损伤指数无减少（或降低）作用。结论姜油对实验性胃溃疡具有一定保护作用,但其作用机制可能不是通过抑制胃酸分泌、胃蛋白酶活性而发挥。     

姜辣素对动物实验性胃溃疡的影响

目的考察姜辣素抗小鼠胃溃疡作用并初步探讨其作用机制。方法采用幽门结扎法致小鼠胃溃疡模型和阿司匹林致胃溃疡模型,判定胃黏膜损伤指数;收集胃液,测其胃液量,总酸度,胃蛋白酶活性及游离黏液量,胃壁结合黏液量及6-酮前列腺素F1α(6-keto-prostaglandin F1α,6-keto-PGF1α)的含量。结果姜辣素能减少幽门结扎和阿司匹林致胃黏膜损伤指数,对胃液分泌有抑制作用,可以显著降低胃液总酸度。但对胃蛋白酶无显著影响。对胃液中游离黏液和胃壁结合黏液的分泌有显著地促进作用。并能显著增加6-keto-PGF1α的含量。结论姜辣素具有一定的抗胃溃疡的作用,其机制可能与增加前列腺素E2(prostaglandin E2,PGE2)合成有关。     

壳聚糖对损伤大鼠胃壁细胞的保护作用

目的 研究壳聚糖对损伤大鼠急性胃壁细胞的保护作用.方法 采用大鼠幽门结扎法建立大鼠损伤模型,并与对照组比较.结果 (1)实验组胃内游离酸和总酸度显著低于对照组(P<0.05);(2)实验组的iNOS表达显著高于对照组(P<0.01);(3)电镜下实验组壁细胞旱静息状态,对照组壁细胞呈分泌状态.结论 壳聚糖处理可明显减轻大鼠幽门结扎所致的胃壁细胞损伤,对胃黏膜具有很好的保护作用.     

PTICE预防幽门结扎大鼠胃溃疡及其作用机制

目的研究河纯Ⅰ型胶原蛋白提取物（PTCE）对幽门结扎模型大鼠胃溃疡的影响，探讨其抗溃疡初步作用机制。方法Shay法制备幽门结扎大鼠胃溃疡模型；滴定法测定胃液游离酸和总酸；阿尔新蓝法测定胃黏液糖蛋白含量；放免法测定血清胃泌素含量。结果PT／CE灌胃0．3、0．6或1．2g／kg4d可显著抑制幽门结扎大鼠胃溃疡发生、抑制胃液、胃液游离酸和总酸分泌，显著降低血清胃泌素水平，和显著升高胃黏膜黏液糖蛋白含量，与幽门结扎病理组比较有显著统计学意义（P〈0．01或P〈0．05）。结论 PTICE抗消化性溃疡和胃黏膜保护作用，与其抑制胃泌素和胃酸分泌，促进胃黏膜黏液糖蛋白分泌或生成有关。     

关苍术超临界提取物对乙醇致大鼠胃黏膜损伤保护作用的研究

目的:研究关苍术超临界提取物(GCT)对乙醇致大鼠胃黏膜损伤的保护作用。方法:40只Wistar大鼠均分成5组,即空白对照(等容蒸馏水)、模型(等容蒸馏水)、铝碳酸镁(0.37g.kg-1)和GCT高、低剂量(0.70、0.35g.kg-1)组。ig给药,每天1次,连续5d,末次给药30min后ig无水乙醇(0.5mL.100g-1)复制急性胃黏膜损伤模型,观察胃黏膜损伤面积,测定胃组织中丙二醛(MDA)、一氧化氮(NO)含量和超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)、一氧化氮合成酶(NOS)活性及环氧化物酶2(COX-2)蛋白表达水平。结果:高、低剂量GCT能显著抑制乙醇引起的大鼠胃黏膜损伤及胃组织中MDA含量的增加和MPO活性的升高,抑制SOD活性的减弱、NO含量和NOS活性的降低,并抑制COX-2蛋白的表达。结论:GCT能拮抗乙醇引起的胃黏膜损伤,其机制可能与通过抑制氧自由基产生、维持胃黏膜中NO正常水平、下调COX-2表达有关。     

银杏叶提取物的胃粘膜保护作用(英文)

目的:研究银杏叶提取物的胃粘膜保护作用.方法:采用大鼠束缚-冷冻应激(RCS)模型和小鼠无水乙醇损伤模型观察GbE对胃粘膜损伤指数的影响;采用幽门结扎法收集胃液,观察GbE对胃液分泌量,胃液酸度和胃蛋白酶活性的影响;采用硫代巴比妥酸(TBA)法测定胃粘膜及血清中丙二醛(MDA)含量.结果:GbE(25,50,100 mg/kg,bid×5 d,ig)剂量依赖性地抑制RCS和无水乙醇引起的胃粘膜损伤.用药组应激后的胃粘膜损伤指数分别为对照组的58％,43％和31％;用药组乙醇诱发的胃粘膜损伤指数降至对照组的62％,36％和26％;GbE尚能增强西米替丁对胃粘膜的保护作用,但对大鼠胃液分泌量、胃液酸度及胃蛋白酶活性GbE并无明显影响.小鼠经无水乙醇ig后1 h,胃粘膜和血清中的MDA含量显著升高(P<0.01),而GbE(25,50,100 mg/kg,ig)预处理则可以明显抑制MDA的升高.结论:GbE具有胃粘膜保护作用,并且与西米替丁在治疗急性胃粘膜损伤方面具有协同作用.     

竹叶黄酮对乙醇诱导小鼠急性胃黏膜损伤的保护作用

目的观察竹叶黄酮对乙醇诱导小鼠急性胃黏膜损伤的保护作用。方法取40只小鼠随机均分为对照组、模型组、维生素E(50 mg/kg)组以及竹叶黄酮25、50 mg/kg组。各组连续ig给药7 d,1次/d。末次给药1 h后,各组按10 mg/kg ig给予无水乙醇,制作胃黏膜损伤模型。建模4 h后,观察胃黏膜损伤面积,计算胃黏膜损伤指数和损伤抑制率。测定小鼠胃黏膜组织中一氧化氮(NO)、前列腺素(PEG2)含量以及血清中超氧化物歧化酶(SOD)、丙二醛(MDA)水平。结果与模型组比较,竹叶黄酮25 mg/kg组小鼠胃黏膜损伤面积减少,50 mg/kg组小鼠损伤程度最小。与模型组比较,竹叶黄酮25、50 mg/kg组小鼠胃黏膜损伤指数均明显降低(P0.01);胃黏膜组织NO、PEG_2含量明显升高(P0.01);血清SOD、MDA水平明显降低(P0.01),SOD/MDA比值明显升高(P0.01)。结论竹叶黄酮能拮抗乙醇诱导的胃黏膜损伤,其机制可能与其抗氧化、抑制氧自由基产生并升高胃黏膜NO、PEG_2含量有关。     

五种不同基源石斛对小鼠胃粘膜损伤的保护作用及机制研究

目的:研究叠鞘、金钗、铁皮、马鞭和鼓槌石斛对小鼠乙醇性胃粘膜损伤的保护作用及其与氧自由基(OFR)、一氧化氮(NO)和前列腺素(PG)的关系.方法:制备小鼠乙醇性胃粘膜损伤模型,测定胃粘膜损伤指数;测定胃组织内SOD、MDA、NO和PGE2含量.结果:石斛可剂量依赖性地抑制无水乙醇诱发的小鼠胃粘膜损伤,使小鼠胃粘膜损伤过程中胃组织中升高的MDA含量降低,使降低的SOD活性和NO水平回升,对胃组织中PGE2含量无明显影响.结论:石斛对小鼠乙醇性胃粘膜损伤具有保护作用,其作用机制与石斛抗氧化作用有关,叠鞘石斛可能与促进NO水平恢复正常也有关系.     

Anti-ulcer activity and mode of action of the polysaccharide fraction from the leaves of Panax ginseng.

The effects of a weakly acidic polysaccharide fraction, GL-4, from the leaves of Panax ginseng C. A. Meyer on various experimental gastric ulcer models in mice and rats have been studied. Oral administration of GL-4 at doses of 50 to 200 mg/kg inhibited the formation of the gastric lesions induced by necrotizing agents such as HCl/ethanol and ethanol in a dose-dependent manner. This protective effect was observed not only upon oral but also upon subcutaneous administration of GL-4 (50-100 mg/kg). GL-4 also inhibited the formation of gastric ulcers which were induced by water immersion stress, indomethacin, or pylorus-ligation. The contents of prostaglandin E2 in the gastric juice from rats were not influenced by oral administration of GL-4. The protective action of GL-4 against HCl/ethanol-induced gastric lesions was not abolished by pretreatment with indomethacin. When GL-4 (100 mg/kg, p.o.) was administered into pylorus-ligated rats, both gastric acidity and pepsin activity in the gastric juice decreased significantly.     

Paracetamol confers resistance to ethanol-induced gastric mucosal damage in rats

Paracetamol given orally or subcutaneously did not produce any observable gastric mucosal damage, nor did it change the acidity of the residual secretion in rat stomachs. However, it delayed the gastric emptying rate and increased the residual volume of gastric secretion. Pretreatment with paracetamol 250 mg kg-1 significantly prevented ethanol-induced gastric ulceration. Although it did not influence ethanol-stimulated acid secretion, it increased the mucosal mucus content in the ethanol-treated animals. The findings suggest that the protective mechanism of paracetamol against ethanol-induced damage is likely to be due to improved gastric mucosal integrity, through an increase in the adherent mucosal mucus which protects the underlying delicate cellular structures.     

Protection of gastric mucosal damage by Coriandrum sativum L. pretreatment in Wistar albino rats

The effect of Coriander pretreatment on gastric mucosal injuries caused by NaCl, NaOH, ethanol, indomethacin and pylorus ligation accumulated gastric acid secretions was investigated in rats. Pretreatment at oral doses of 250 and 500mg/kg, body weight was found to provide a dose-dependent protection against the (i) ulcerogenic effects of different necrotizing agents; (ii) ethanol-induced histopathological lesions; (iii) pylorus ligated accumulation of gastric acid secretions and ethanol related decrease of Nonprotein Sulfhydryl groups (NP-SH). Results obtained on the study of gastric mucus and indomethacin-induced ulcers demonstrated that the gastro protective activity of Coriander might not be mediated by gastric mucus and/or endogenous stimulation of prostaglandins. The protective effect against ethanol-induced damage of the gastric tissue might be related to the free-radical scavenging property of different antioxidant constituents (linanool, flavonoids, coumarins, catechins, terpenes and polyphenolic compounds) present in Coriander. The inhibition of ulcers might be due to the formation of a protective layer of either one or more than one of these compounds by hydrophobic interactions.     

Protective effect of butyrate against ethanol-induced gastric ulcers in mice by promoting the anti-inflammatory,anti-oxidant and mucosal defense mechanisms

Gastric ulcers (GUs) are a common type of peptic ulcer. Alcohol overdose is one of the main causes of GU, which is difficult to prevent. Although the protective effect of butyrate on inflammation-related diseases is well understood, its effect on GUs has not been reported. We investigated the protective effects of butyrate against ethanol-induced lesions to the gastric mucosa in mice and the underlying mechanisms. BALB/c mice were orally pretreated with butyrate for 30 min prior to the establishment of the GU model by challenge with absolute ethanol. Ethanol administration produced apparent mucosal injuries with morphological and histological damage, whereas butyrate pretreatment reduced the gastric mucosal injuries in a dose-dependent manner. Butyrate pretreatment also significantly ameliorated contents of malondialdehyde (MDA) and carbonyl proteins, and decreased levels of IL-1β, TNF-α and IL-6. The Western blot results consistently demonstrated that butyrate pretreatment attenuated the phosphorylation of NF-κB p65, p38 MAPK and ERKs in the gastric tissues. Additionally, gastric wall mucus (GWM), a parameter reflecting mucosal defense, was clearly increased by butyrate pretreatment. Butyrate pretreatment protects the gastric mucosa against ethanol-induced lesions by strengthening the mucosal defense and anti-oxidant and anti-inflammatory activities. As a necessary substance for the body, butyrate may be applied to the prevention and treatment of GUs.     

Antiulcer activity and the mechanism of action of magaldrate in gastric ulceration models of rat

The present study was undertaken to investigate the mechanism of cytoprotective effects of magaldrate in aspirin plus pylorus-ligation model and ethanol-induced gastric ulcer model in rats. Magaldrate (60 mg/kg, p.o.) produced a significant reduction in the ulcer index and significant increase in mucus content in ethanol-induced gastric ulceration in rats. In aspirin plus pylorus-ligation model magaldrate produced significant decrease in ulcer index, total acidity and protein content (PR). It did not produce any significant change in volume of gastric secretion. However, it produced significant increase in total carbohydrate (TC) level but not in ratio between TC and proteins. It also produced a significant decrease in lipid peroxidation (as expressed by thiobarbituric acid reactive substance). Our data suggests the cytoprotective action of magaldrate on gastric mucosal cells which may be due to protection of gastric mucosa from lipid peroxidation.