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。     

胃康胶囊对消炎痛诱导大鼠胃粘膜损伤血液中相关细胞因子含量的影响

目的：观察胃康胶囊对消炎痛引起的大鼠急性胃粘膜损伤时血液中相关细胞因子[前列腺环素（PGI2）、血小板活化因子（PAG）、肿瘤坏死因子－α（TNF-α）、表皮生长因子（EGF）]含量的影响，探讨其在保护胃粘膜损伤过程中的分子机制。方法：Wistar大鼠30只灌胃给药1周后，用消炎痛复制成急性胃粘膜损伤模型，5h后处死大鼠进行以上血液相关细胞因子的检测。结果：胃康胶囊能降低急性胃粘膜损伤大鼠血液中PAF、TNF-α的含量，升高PGI2，EGF的含量，对抗胃酸分泌增加，结论：胃康胶囊对消炎痛引起的大鼠胃粘膜损伤有保护作用。对胃溃疡有预防作用。     

益气化瘀煎剂抗大鼠胃溃疡作用及其机制的探讨

目的：研究益气化瘀煎剂对大鼠实验性胃溃疡的防治作用,并对其机制进行探讨。方法：观察预先应用中药对应激、乙醇、消炎痛、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8、18和26d后,醋酸性胃粘膜损伤的愈合情况;检测胃壁结合粘液、胃组织DNA、胃粘膜超氧化物歧化酶（SOD）、丙二醛（MDA）及前列腺素E2（PGE2）的含量。结果：益气化瘀煎剂显著抑制应激、乙醇及消炎痛性胃粘膜损伤（P＜0．05,＜0．01）,并具有剂量依赖关系;加速胃溃疡的愈合。其疗效与雷尼替丁接近。同时,增加胃粘膜组织DNA、SOD及PGE2的含量,减低MDA的生成。结论：益气化瘀煎剂具有较强防治胃溃疡的作用,其机制可能主要是增强胃粘膜细胞保护作用。     

胃舒胶囊治疗大鼠萎缩性胃炎癌前病变的作用机制

目的：探讨胃舒胶囊对大鼠萎缩性胃炎癌前病变的作用机制。方法：采用甲硝基亚硝基胍造成大鼠萎缩性胃炎癌病变模型。将造模大鼠随机分为正常组、模型组、维甲酸组、胃舒胶囊组,观察血清过氧化脂质（LPO）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH－Px)、胃粘膜病理形态及组织超微结构变化。结果：模型组大鼠血清LPO含量升高,SOD及GSH－Px活性下降;病理检查显示胃粘膜固有腺体减少,纤维组织增生,膜肌增厚,腺体化生,异型增生,胃小凹延长,增殖细胞数、AgNOR颗粒数显著增多;超微结构亦有明显变化。与模型组比较,胃舒胶囊组显著改善（P＜0．01－0．05）。结论：胃舒胶囊可抑制大鼠胃粘膜上皮细胞的异常增殖;增强抗氧化能力,减轻自由基对胃粘膜上皮细胞的损伤和致癌致突变作用。     

苍脂颗粒剂对鼠胃粘膜细胞保护作用的研究

为了探讨苍脂颗粒剂治疗脾胃病的胃粘膜保护作用，采用利血平模拟的大鼠脾虚证及亚急性阿斯匹林胃粘膜损伤模型，测定其对非蛋白质流基物质（NPSH）、谷胱甘肽过氧化物酶（GSH－px）、过氧化氢酶（CAT）、超氧化物歧化酶（SOD）及血浆过氧化脂质（LPO）等具有胃粘膜细胞保护作用物质的含量或活性的影响。结果显示，苍脂颗粒剂可以明显改善脾虚伴慢性胃粘膜病变大鼠及亚急性阿期匹林胃粘膜损伤大鼠的粘膜损伤程度，显著提高胃粘膜NPSH（F＜0．01）、GSH-px（P＜0．01）等细胞保护物质的水平．提示苍脂颗粒剂具有一定的胃粘膜细胞保护作用。     

奥美拉唑对大鼠胃粘膜保护作用的研究

目的：探讨奥美拉唑对大鼠胃粘膜的保护作用。方法：在乙醇诱导大鼠胃粘膜损伤前，预先给予奥美拉唑、L－硝基－精氨酸甲酯（L－NAME）静脉注射。测定胃粘膜血流量（GMBF）、胃液pH和胃粘膜NO2^-/NO3^-含量，并观察胃粘膜损伤指数（Ulcer index ,UI)、溃疡坏死组织和中性粒细胞浸润严重程度的变化。结果：与模型损伤组比，奥美拉唑组大鼠UI明显降低（P＜0．01），溃疡坏死组织和中性粒细胞浸润程度明显减轻（P＜0．01）。预先用L－NAME处理后，奥美拉唑保护胃粘膜损伤的作用明显减弱。静脉注射奥美拉唑，可增加GMBF和胃粘NO2^-/NO3^－含量，L－NAME可逆转这种作用，但对奥美拉唑抑制酸分泌作用无明显影响。结论：奥美拉唑对大鼠胃粘膜具有重要的保护作用，一氧化氮介导了这种作用。     

丹参对大鼠肝硬化门脉高压缺血再灌注胃粘膜损伤的实验研究

实验制成大鼠肝硬化门脉高压（PHT）缺血再灌注模型，用电子自旋共振技术测定缺血再灌注前后及丹参治疗后胃粘膜中氧自由基（OFR）以及脂质过氧化物（LPO）和超氧化物歧化酶（SOD）的变化，同时光镜、电镜观察其病理改变，探讨丹参对胃粘膜再灌注损伤的防治作用。实验结果提示：PHT胃粘膜较正常胃粘膜更易受缺血再灌注损伤，粘膜损伤的严重程度与OFR、LPO及SOD密切相关；早期使用丹参可显著降低胃粘膜中OFR及LPO含量，提高SOD活性，减轻胃粘膜掼伤，起到保护胃粘膜的作用。     

硫氧还蛋白系统在冰泳负荷致低硒大鼠心肌氧化损伤中的作用

目的探讨硫氧还蛋白(Trx)系统在低硒心肌氧化损伤中的作用并分析其机制。方法复制大鼠低硒模型，给予冰泳负荷，用光镜观察心肌形态改变，用Western blot检测心肌组织中硫氧化还原蛋白表达变化，检测血中脂质过氧化物(LPO)含量及心肌TR活性。结果低硒组大鼠血中LPO含量较常硒组增高，低硒加冰泳负荷后LPO增加更明显，并导致大鼠心肌细胞坏死和炎细胞浸润；常硒冰泳组大鼠心肌硫氧化还原蛋白还原酶(TR)活性和Trx表达升高；低硒冰泳组大鼠心肌TR活性和Trx蛋白表达较负荷前改变不明显。结论低硒条件下心肌Trx系统功能降低，遇到冰泳负荷时心肌不能及时清除过剩的自由基及修复损伤的蛋白，导致心肌抗氧化能力降低，使心肌易受损伤。     

植物油乳治疗胃溃疡的实验与临床研究

目的：对两种植物油乳──鸦胆子油乳（简称鸦乳）和豆油乳治疗胃溃疡的作用进行观察。方法：首先观察鸦乳对四种胃溃疡动物模型的疗效，进而探讨其对动物胃粘膜内源性PGE2、MDA、SOD活性和氧自由基相对含量的影响，然后通过开放性临床观察和随机双盲对照试验观察其临床疗效。结果：鸦乳对四种胃溃疡动物模型均有疗效（P＜0．01）；豆油乳对应激性胃溃疡动物模型亦有疗效，作用与鸦乳比较，差异无显著性（P＞0．05）；鸦乳增加动物及人体胃粘膜内源性PGE2（P＜0．01），降低动物胃粘膜SOD活性（P＜0．01），减低动物胃粘膜MDA和氧自由基相对含量（P＜0．01）。开放性临床观察及随机双盲对照临床观察均显示，鸦乳治疗胃溃疡的8周有效率＞91．62％，8周愈合率＞75％，疗效优于对照剂西咪替丁（国产）和石蜡油乳（P＜0.01），未发现不良反应。结论：鸦乳和豆油乳治疗胃溃疡的疗效是肯定的，其主要作用机理是增加胃粘膜内源性PGE2、减轻氧自由基对胃粘膜的损害。     

电针抗应激性胃溃疡大鼠脑组织和胃粘膜中一氧化氮合酶的变化

观察应激性胃溃疡大鼠脑组织和胃粘膜中一氧化氮合酶（NOS）活性的变化．并对电外足三里穴和阳陵泉穴NOS的变化及与胃粘膜损伤的关系作了比较。结果发现,应激性胃溃疡大鼠脑组织和胃粘膜NOS均增高，尤其是胃粘膜NOS增高非常显著（P＜0.01）；电针足三里使脑和胃NOS回降，应激前先电针更为明显，使胃溃疡损伤指数显著下降（P＜0.01）；而电针阳陵泉．与应激组相比虽也下降，但无统计学意义。提示NOS参与了电针对应激所致胃粘膜损伤的保护．这种保护作用可能与中枢和肠神经系统对胃功能的双重调节有关，同时NOS的变化与电针胃经足三里穴位特异性有一定的联系。     

Determination of lipid peroxide and superoxide dismutase in blood and tissueof patients with gastrointestinal cancer

AIM To study the relationship between the lipid peroxide (LPO) and superoxide dismutase (SOD) and thepathogenesis of gastrointestinal cancers.METHODS We investigated the SOD activity and LPO levels in blood and mucosa of patients withesophageal (EC), gastric (GC) and colorectal cancer (CC), gastric ulcer (GU) and compared with normalesophagus (NE), stomach (NS) and colon (NC). respectively, 287 patients who underwent endoscopy werestudied. SOD activity of the tissue and blood was determined using SUN's adrenaline auto oxidation method.LPO levels were determined according to YU's method.RESULTS The SOD activity and LPO level in blood and mucosa are shown in the Table 1 (x±Sx). Table 1 SOD and LPO in blood and tissues of patients with gastrointestinal cancers SOD(U／mg protein) LPO(U／mg) Groups n Tissue blood Tissue Blood Normal stomach Gastric ulcer Gastric cancer Normal esophagus Esophageal cancer Normal colon Colon cancer 60 42 43 32 52 28 30 1.90±0.18 0.64±0.40a 0.37±0.24a 1.17±0.70 0.39±0.30a 0.81±0.36 0.31±0.17b 33.70±1.73 25.50±0.67b 27.86±1.02b 30.80±3.78 28.23±10.63 20.97±4.77 19.35±7.32 0.01±0.004 0.05±0.010b 0.06±0.021b 0.014±0.005 0.061±0.033b 0.012±0.003 0.069±0.015b 0.83±0.01 0.11±0.02 0.12±0.03 0.08±0.02 0.11±0.02 0.08±0.03 0.11±0.02 aP<0.001, bp<0.01 vs corresponding normal controls, respectively. CONCLUSION SOD activity of the tissue is significantly decreased in EC. GC and CC. LPO levels weresignificantly higher than those of corresponding normal tissue. These results suggest that mucosal SOD andLPO levels are closely related to the pathogenesis of the gastrointestinal cancers.     

硝苯啶治疗消化性溃疡的疗效及其机理探讨

用硝苯碇预防无水乙醇和幽门结扎所致大鼠胃溃疡，结果显示用药组胃溃疡指明显低于对照组，对溃疡的抑制率与ＮＦＤ剂量呈正相关。临床观察４２例十二指肠球部溃疡患者，服用ＮＦＤ １０ｍｇ，每日４次，６周后溃疡愈合２７例，总有效３９例，与对照比较有显著差异。     

胃舒合剂对大鼠乙酸实验性胃溃疡的保护作用及其机理探讨

本实验发现大鼠乙酸实验性胃溃疡模型，存在着血液流变学的异常和自由基反应的失衡，其全血比粘度及全血还原粘度高于正常组（Ｐ＜０．０１），血浆超氧阴离子、红细胞超氧阴离子，血过氧化脂质（ＬＰＯ）也明显高于正常组（Ｐ＜０．０１），血过氧化物歧化酶（ＳＯＤ）则低于正常组（Ｐ＜０．０１）。中药胃舒合剂可明显地改善大鼠血液流变学的异常及氧自由基的失衡，对乙酸所致的大鼠实验性胃溃疡有显著的保护作用，且其作用优于三九胃泰（Ｐ＜０．０１）。     

慢性浅表性胃炎和消化性溃疡患者人表皮生长因子含量的检测意义初探

目的：了解人类表皮生长因子（ｈＥＧＦ）与胃粘膜完整性的关系。方法：用放免法检测正常人、慢性浅表性胃炎（活动期）、消化性溃疡（愈合期）等四组病人血、尿、胃液中的ｈＥＧＦ含量。结果：慢性浅表性胃炎（活动期）和消化性溃疡（活动期）病人上述三种体液中的ｈＥＧＦ含量明显低于正常人和消化性溃疡（愈合期）病人（Ｐ〈０．０５），而正常人与消化性溃疡（愈合期）病人的ｈＥＧＦ含量无明显差别（Ｐ〉０．０５）。结论：说明     

Protective Effect of a Vasopressin-1 Selective Antagonist, OPC-21268, Against Ethanol-Induced Damage of The rat Gastric Wall

Since endogenous vasopressin has been reportedto be an aggressor in the gastric mucosa and avasoconstrictor in the gastric circulation, weinvestigated the gastric cytoprotective effects ofOPC-21268, a newly developed, nonpeptide, orally activevasopressin-1 receptor antagonist, on ethanol-inducedgastric injury in rats. The rats were treated withOPC-21268 or placebo 2 hr before ethanol administration, and the gastric mucosa was evaluatedmacroscopically for ulcer damage, and histologically forgastric mucosal injury. Gastric mucosal blood flow,erythrocyte volume, and erythrocyte velocity were alsomeasured in groups given saline, ethanol alone, andethanol after OPC-21268. To investigate the role ofsystemic or locally secreted vasopressin, we measuredplasma and tissue (gastric mucosa) vasopressinconcentrations after ethanol or vehicle administration.Prophylactic OPC-21268 treatment improved the gastriculcer score in a dose-dependent manner, and histologicalexamination demonstrated that the drug significantly ameliorated the gastric injury induced byethanol. The hemodynamic values obtained in theOPC-21268-treated and ethanol-treated group were similarto those in the saline control group, but values weresignificantly (P < 0.05) higher for gastric mucosal bloodflow and erythrocyte velocity and lower for erythrocytevolume compared to the group given ethanol alone. Plasmavasopressin concentrations were not significantly different in the control group and at 15, 30,and 60 min after administration of ethanol. However,ethanol administration caused a threefold increase ingastric tissue vasopressin level (P < 0.05) compared to the control group. These results suggestedthat OPC-21268 relieved congestive hyperemia in thegastric mucosa and ameliorated the mucosal injury causedby ethanol, probably as a result of inhibition of vasopressin-mediated actions on the stomach.The vasopressin involved was probably generated locallyin the gastric mucosa after ethanoladministration.     

The Role of Zinc Sulfate and Metallothionein in Protection Against Ethanol-Induced Gastric Damage in Rats

In this study, the effects of zinc sulfate against ethanol-induced acute gastric damage in rats were investigated, morphologically and biochemically. In addition, the present investigation has demonstrated the distribution of metallothionein stimulated by zinc in gastric mucosal tissues, immunohistochemically. The gastric damage was induced by intragastric administration of 1 ml absolute ethanol per rat. Rats received zinc sulfate (100 mg/kg/day) for 3 consecutive days 2 hr prior to the administration of absolute ethanol. Acute ethanol exposure caused degenerative morphological changes, a decrease in metallothionein immunreactivity; an increase in lipid peroxidation (LPO) levels, and a decrease in reduced glutathione (GSH) levels in gastric mucosa. On the other hand, zinc sulfate administration to ethanol-treated rats caused a significant reduction in the histological damage, an increase in metallothionein immunreactivity, a decrease in LPO levels, and an increase in GSH levels in gastric mucosa. As a result, the present study indicates that zinc sulfate has a protective effect against ethanol-induced acute gastric damage. In addition, we might say that the zinc given as exogenous protection against acute gastric damage has a protective effect both by stimulation of metallothionein synthesis and through GSH as well as having antioxidative potential.     

Gastroprotective activity of Nigella sativa L oil and its constituent, thymoquinone against acute alcohol-induced gastric mucosal injury in rats

AIM: To evaluate the role of reactive oxygen species in the pathogenesis of acute ethanol-induced gastric mucosal lesions and the effect of Nigella sativa L oil (NS) and its constituent thymoquinone (TQ) in an experimental model. METHODS: Male Wistar albino rats were assigned into 4 groups. Control group was given physiologic saline orally (10 mL/kg body weight) as the vehicle (gavage); ethanol group was administrated 1 mL (per rat) absolute alcohol by gavage; the third and fourth groups were given NS (10 ml/kg body weight) and TQ (10 mg/kg body weight p.o) respectively 1 h prior to alcohol intake. One hour after ethanol administration, stomach tissues were excised for macroscopic examination and biochemical analysis. RESULTS: NS and TQ could protect gastric mucosa against the injurious effect of absolute alcohol and promote ulcer healing as evidenced from the ulcer index (UI) values. NS prevented alcohol-induced increase in thiobarbituric acid-reactive substances (TBARS), an index of lipid peroxidation. NS also increased gastric glutathione content (GSH), enzymatic activities of gastric superoxide dismutase (SOD) and glutathione-S-transferase (GST). Likewise, TQ protected against the ulcerating effect of alcohol and mitigated most of the biochemical adverse effects induced by alcohol in gastric mucosa, but to a lesser extent than NS. Neither NS nor TQ affected catalase activity in gastric tissue. CONCLUSION: Both NS and TQ, particularly NS can partly protect gastric mucosa from acute alcohol-induced mucosal injury, and these gastroprotective effects might be induced, at least partly by their radical scavenging activity.     

Micronutrient antioxidants in gastric mucosa and serum in patients with gastritis and gastric ulcer: does Helicobacter pylori infection affect the mucosal levels?

Free radicals (FRs) play an important role in the pathogenesis of gastroduodenal mucosal inflammation, peptic ulcer disease, and probably even gastric cancer. Various micronutrients protect the gastric mucosa by scavenging FRs. Only limited data is available regarding the concentration of micronutrients in the gastric mucosa in patients with gastritis and peptic ulcer disease. Our aim was to analyze micronutrient antioxidant concentrations in the antral mucosa in patients with gastritis and gastric ulcer and to determine the influence of Helicobacter pylori infection on gastric mucosal antioxidants in patients with gastritis and gastric ulcer. Patients who underwent upper endoscopy for evaluation of dyspepsia were included in the study. Ascorbic acid, alpha-tocopherol, alpha-carotene, beta-carotene, total carotenoids, lutein, cryptoxanthin, and lycopene levels were measured in the sera and antral mucosal biopsies in these patients. The diagnosis of H. pylori was confirmed by histology, urease test (CLO) and serology. Patients with negative endoscopic findings and normal histology and no H. pylori infection served as controls. In patients with gastritis, alpha-tocopherol levels were reduced in serum and mucosa irrespective of H. pylori status, whereas carotenoids and ascorbic acid levels were similar to controls. However, in patients with gastric ulcer, serum and mucosal levels of all micronutrient antioxidants were markedly decreased compared with both controls and patients with gastritis. The degree of depletion of antioxidants was similar in patients with either H. pylori-induced or nonsteroidal antiinflammatory drug (NSAID)-induced ulcers. Patients with gastric ulcer have very low gastric antioxidant concentrations compared to patients with gastritis and normal mucosa. This depletion in antioxidants seems to be a nonspecific response and was not related to H. pylori infection.     

Protection of gastric mucosa from ethanol induced injury by recombinant epidermal growth factor in rats

ＮＴＲＯＤＵＣＴＩＯＮＥｐｉｄｅｒｍａｌｇｒｏｗｔｈｆａｃｔｏｒ（ＥＧＦ）ｉｓａｓｉｎｇｌｅｃｈａｉｎｐｏｌｙｐｅｐｔｉｄｅｔｈａｔｉｓｓｅｃｒｅｔｅｄｂｙｓｕｂｍａｎｄｉｂｕｌａｒａｎｄＢｒｕｎｎｅｒ′ｓｇｌａｎｄｓａｎｄｉｓａｐｏｗｅｒｆｕｌｍ...