荆花胃康胶丸对胃溃疡大鼠胃黏膜的促愈合作用

目的:观察荆花胃康胶丸对实验性胃溃疡大鼠胃黏膜的促愈合作用。方法:100只SD大鼠建立胃溃疡模型,随机分成模型对照(给予生理氯化钠溶液)组、雷尼替丁30 mg·kg~(-1)·d~(-1)组、荆花胃康胶丸10,15和20 mg·kg~(-1)·d~(-1)组,每组20只,另取20只正常大鼠作为正常对照组。在造模后d 5各组开始灌胃给药或生理氯化钠溶液,bid,连续14 d。用游标卡尺测量溃疡指数(ulcer index,UI),用硝酸还原酶法测定胃黏膜NO含量,用ELISA法检测胃黏膜表皮生长因子(EGF)含量,用SABC免疫组化的方法检测胃黏膜表皮生长因子受体(EGFR)的表达。结果:与模型组比较,荆花胃康胶丸组UI值剂量依赖性的降低,血清和组织NO和EGF含量剂量依赖性的升高。荆花胃康胶丸组溃疡边缘组织EGFR阳性表达的细胞较模型组和正常对照组增多(P＜0．01)。结论:荆花胃康胶丸可能通过促进胃黏膜NO和EGF分泌,维持胃黏膜结构完整;通过上调上皮细胞EGFR表达,加速溃疡愈合。     

荆花胃康胶丸对溃疡大鼠胃黏膜及6-keto-PGF1α含量的影响

目的研究荆花胃康胶丸对Okabe氏溃疡模型大鼠胃黏膜愈合及溃疡组织6-酮-前列腺素F1α(6-keto-PGF1α)含量的影响.方法采用Okabe氏法,在大鼠胃前壁造成溃疡,随机将模型动物分为模型对照(生理氯化钠溶液)、荆花胃康胶丸大、中、小剂量(30,20,10 mg·kg-1·d-1)、硫糖铝10 mg·kg-1·d-1及法莫替丁5 mg·kg-1·d-1组,各组均灌胃给药,qd,连续10 d.给药结束后,计算各组大鼠溃疡面积和溃疡指数,测定溃疡组织黏膜缺损宽度及再生黏膜厚度,并定量检测胃组织的6-keto-PGF1α含量.结果与模型对照组相比,荆花胃康胶丸组剂量依赖性地降低溃疡面积和溃疡指数及黏膜肌层缺损宽度,增加再生黏膜厚度和大鼠胃组织6-keto-PGF1α的含量(P＜0.01);荆花胃康胶丸30 mg·kg-1组的作用优于硫糖铝组及法莫替丁组(P＜0.05).结论荆花胃康胶丸能促进溃疡愈合,其机制可能与增加溃疡组织6-keto-PGF的含量有关.     

荆花胃康胶丸对阿司匹林致小鼠胃黏膜损伤的修复作用

目的:探讨中药荆花胃康胶丸对阿司匹林所致小鼠胃黏膜损伤的修复作用.方法:建立阿司匹林所致小鼠急性胃黏膜损伤模型,观察中药荆花胃康胶丸(30mg·kg-1,ig)与胶体果胶铋胶囊(130mg·kg-1,ig)对胃黏膜损伤的修复作用,计算溃疡指数和溃疡抑制率.结果:中药荆花胃康胶丸能明显缩小阿司匹林烧灼引起的溃疡面积,溃疡指数较单纯损伤组显著降低(P＜0.05);与胶体果胶铋组比较,胃黏膜溃疡指数和溃疡抑制率无明显差异,保护作用相当.结论:中药荆花胃康胶丸对阿司匹林所致的小鼠胃黏膜损伤有较好的修复作用.     

和胃冲剂对大鼠急性胃黏膜损伤的保护作用

目的：观察中药复方和胃冲剂对大鼠急性胃黏膜损伤的保护作用。方法：将40只健康♂性Spaque-Dawley大鼠随机分为5组：正常对照纽、模型对照组、和胃冲剂低、中、高剂量组，采用无水乙醇诱导大鼠急性胃黏膜损伤，分别测定各组大鼠的胃黏膜损伤指数、血浆超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量，并在光镜下观察胃黏膜病理学改变。结果：和胃冲剂各剂量组的损伤指数较模型对照组显著降低（P〈0．01），且呈剂量依赖性；血浆中SOD活性显著升高，MDA含量下降，黏膜损伤程度明显减轻。结论：和胃冲剂对无水乙醇诱导的急性胃黏膜损伤有明显的保护作用，其机制可能与抗氧化作用有关。     

荆花胃康胶丸对溃疡大鼠胃黏膜NO,NOS和ET含量的影响

目的:观察荆花胃康胶丸对溃疡大鼠胃黏膜内皮素(ET)、一氧化氮(NO)、一氧化氮合酶(NOS)含量的影响。方法:采用Okabe氏法造成大鼠胃溃疡模型,随机将模型动物分为蒸馏水对照组、荆花胃康胶丸30,20, 10 mg·kg~(-1)·d~(-1)组、硫糖铝10 mg·kg~(-1)·d~(-1)及法莫替丁5 mg·kg~(-1)·d~(-1)组,每组8只。各组均灌胃给药,qd,连续10 d。末次给药后次日,测定各组溃疡面积,并测定溃疡周围组织NO,NOS及ET含量。结果:与对照组相比,荆花胃康胶丸30,20,10 mg·kg~(-1)·d~(-1)组的溃疡面积显著降低,溃疡周围组织NO及NOS的含量明显增高,ET的含量明显降低(P＜0．01),且呈现剂量依赖性;荆花胃康胶丸30 mg·kg~(-1)·d~(-1)组的保护作用优于硫糖铝及法莫替丁组(P＜0．05)。结论:荆花胃康胶丸可能通过增加胃溃疡组织NO及NOS的含量及降低ET的含量来发挥胃黏膜修复作用。     

丹佛胃尔康颗粒对大鼠胃黏膜损伤的保护作用研究

目的：对丹佛胃尔康颗粒的抗胃溃疡及保护胃黏膜的作用作出科学的评价。方法：采用幽门结扎法、皮下注射消炎痛及浆膜下注射冰乙酸等方法致大鼠胃溃疡,无水乙醇致大鼠急性胃黏膜损伤,观察丹佛胃尔康颗粒的抗胃溃疡及保护胃黏膜的作用。结果：丹佛胃尔康颗粒对幽门结扎法、皮下注射消炎痛及浆膜下注射冰乙酸等法引起的胃溃疡和无水乙醇所致大鼠急性胃黏膜损伤有明显的抑制作用。结论：丹佛胃尔康颗粒有抗实验性胃溃疡的作用。     

胃得安片对应激性胃损伤模型大鼠胃功能及胃组织中EGF、EGFR表达的影响

目的:研究胃得安片对应激性胃损伤模型大鼠胃功能及胃组织中表皮生长因子(EGF)及其受体(EGFR)表达的影响,探讨其治疗胃溃疡的作用机制。方法:将大鼠随机分为正常组(生理盐水)、模型组(生理盐水)、阳性组(盐酸雷尼替丁,0.015 mg/kg)和胃得安片高、中、低剂量组(1.7、0.87、0.43 g/kg),每组10只。除正常组外,其余各组大鼠均采用空腹冷水游泳法复制胃溃疡模型。成模后,各组大鼠每天ig给药1次,连续2周。记录大鼠于给药第0、7、14天时的体质量;末次给药12 h后,检测大鼠的胃液分泌量、胃液pH值、胃溃疡面积及胃黏膜损伤指数,并检测胃组织中EGF、EGFR的表达。结果:与正常组比较,模型组大鼠给药第7、14天时的体质量及胃液pH值降低,胃液分泌量和胃溃疡面积增加,胃黏膜损伤指数升高,胃组织中EGF、EGFR表达增强,差异均有统计学意义(P<0.05或P<0.01)。与模型组比较,除胃得安片中剂量组大鼠给药第7天时的体质量、胃液分泌量、胃液pH值、胃溃疡面积以及胃得安片低剂量组大鼠给药第7、14天时的体质量、胃液分泌量、胃液pH值、胃溃疡面积改善和胃组织中EGF表达增强不显著外,其余各给药组大鼠上述指标均显著改善,且胃组织中EGF、EGFR表达持续增强(P<0.05或P<0.01);胃得安片的作用呈现一定的量效关系。结论:胃得安片能够显著改善应激性胃损伤模型大鼠的胃功能;其机制可能与增强胃组织中EGF、EGFR表达,从而促进溃疡愈合有关。     

荆花胃康胶丸对实验性胃溃疡及幽门螺杆菌的抑制作用

目的：研究荆花胃康胶丸对实验性胃溃疡及幽门螺杆菌（HP）的抑制作用。方法：应用大、小鼠实验性胃溃疡模型,HP体外敏感性试验和动物胃肠里面动试验,观察荆花胃康预防给药的抗溃疡作用。结果：荆花胃康5－20mg/kg,明显抑制大鼠应激性、幽门结扎型、利血平型和小鼠组胺型胃溃疡,对胃酸和胃蛋白酶活性有显著降低作用,使胃粘液分泌增加;并可促进乙酸型溃愈合,效应与剂量相关,对HP具有强烈抑制作用,MIC为0．024－0．048mg/ml,结论：荆花胃康对实验性胃溃疡及HP有强烈抑制作用。     

辣蓼提取物对大鼠急性胃黏膜损伤的保护作用研究

目的:研究辣蓼提取物对大鼠急性胃黏膜损伤(AGML)的保护作用。方法:将48只大鼠随机分为正常组(生理盐水)、模型组(生理盐水)、阳性组(盐酸雷尼替丁,0.05 g/kg)和辣蓼提取物低、中、高剂量组(以生药量计分别为2.7、8.1、24.3 g/kg),连续灌胃给药7 d,每天1次。末次给药1 h后,除正常组外,其余各组大鼠均灌胃无水乙醇复制AGML模型。造模1.5 h后,计算各组大鼠胃黏膜损伤指数,观察大鼠胃组织病理学变化,采用酶联免疫吸附法测定大鼠胃组织中核因子E2相关因子2(Nrf2)含量和超氧化物歧化酶(SOD)活性。结果:与正常组比较,模型组大鼠胃黏膜损伤明显,黏膜下层毛细血管破裂出血,胃黏膜损伤指数显著升高(P<0.01);胃组织中Nrf2含量和SOD活性显著降低(P<0.05或P<0.01)。与模型组比较,各给药组大鼠胃黏膜的损伤均不同程度减轻;阳性组和辣蓼提取物中、高剂量组大鼠胃黏膜损伤指数显著降低(P<0.05),胃组织中Nrf2含量和SOD活性显著升高(P<0.05或P<0.01)。结论:辣蓼提取物对无水乙醇致大鼠AGML具有较好的保护作用,其机制可能与提高胃黏膜组织中Nrf2含量和增强SOD活性有关。     

胃复宁治疗慢性萎缩性胃炎的实验研究

目的探讨胃复宁治疗慢性萎缩性胃炎（CAG）的部分药效机制。方法通过综合法建立大鼠CAG模型，随机分成胃复宁大剂量组、中剂量组、小剂量组和胶体果胶铋组，检测各组大鼠血清和胃黏膜丙二醛（MDA）、一氧化氮（NO）的变化，观察胃的病理组织学改变。结果模型组血清和胃黏膜MDA、NO以及病理组织学改变与正常组比较有明显差异。胃复宁可明显升高血清和胃黏膜NO（P〈0．01），降低MDA（P〈0．01）；改善CAG的病理状况（P〈0．01）。结论胃复宁可以改善CAG的病理变化，有较强的抗氧化、抑制脂质过氧化作用，能提高胃黏膜NO含量，发挥保护胃黏膜的作用。     

牛乳铁蛋白对实验性胃黏膜损伤及胃溃疡大鼠模型的影响

目的 观察牛乳铁蛋白对实验性大鼠胃黏膜损伤及胃溃疡的保护作用。方法 建立无水乙醇、幽门结扎致大鼠胃黏膜损伤模型,水浸应激、乙酸灼烧致大鼠胃溃疡模型,测定模型大鼠胃黏膜损伤程度、溃疡面积、溃疡指数,以及胃黏膜中氨基己糖、PEG₂含量和血流动力学的变化,观察牛乳铁蛋白对实验性胃黏膜损伤和胃溃疡的保护作用。此外,通过连续喂养正常大鼠牛乳铁蛋白,观察其对大鼠胃液量、胃液酸度和胃蛋白酶活性的影响。结果 牛乳铁蛋白能降低乙醇及幽门结扎致胃黏膜损伤大鼠的溃疡指数,增加乙醇致胃黏膜损伤大鼠受损胃黏膜的氨基己糖和PEG₂含量以及血流量。同时,牛乳铁蛋白还能降低水浸应激以及乙酸灼烧致胃溃疡大鼠胃部的溃疡面积。此外,连续灌胃高剂量牛乳铁蛋白能抑制正常大鼠胃液分泌,减少胃液酸度。结论 牛乳铁蛋白对实验性胃黏膜损伤及胃溃疡大鼠模型胃黏膜损伤具有保护作用。     

蒙脱石散对急性胃黏膜病变的修复作用及其机制

目的:了解蒙脱石散(思密达)对急性胃黏膜病变的修复作用及其机制研究。方法:构建急性胃黏膜病变的SD大鼠模型,将其分为单纯模型组、模型+思密达组、模型+硫糖铝组,以单纯模型组作为阴性对照组,以硫糖铝作为阳性对照组,所有组别大鼠均分别在造模后0,12,24,48,72 h随机立即处死3只,并在肉眼、光镜及电镜下观察各组急性胃黏膜病变的形态学改变,同时监测各时间段各组胃内pH值了解其抗酸作用;监测胃内N-乙酰氨基己糖含量了解其对胃黏液层厚度的影响;监测胃黏膜血流(GMBF)、溃疡指数(UI)、胃黏膜厚度、表皮生长因子(EGF)、一氧化氮(NO)和前列腺素E₁(PGE₁)的表达水平了解其对胃黏膜的修复作用及机理研究。结果:(1)与阴性对照组相比,思密达组急性胃黏膜病变在肉眼、光镜及电镜下均好转。(2)思密达组胃内pH值、胃黏液层厚度、GMBF、胃内N-乙酰氨基己糖含量、NO和PGE₁的表达水平均在至少两个时间段里较阴性对照组有不同程度的升高,且有统计学差异(P<0.05)。结论:思密达对胃黏膜有保护作用。其机制可能与思密达通过升高PGE₁、EGF、NO的表达水平,增加GMBF及糖蛋白含量,从而达到抑酸及增加胃黏膜厚度,降低UI。     

奥美拉唑对大鼠中毒性急性胃黏膜损伤的保护作用及机制

目的：研究不同剂量奥美拉唑对大鼠中毒性急性胃黏膜损伤的保护作用,探讨其保护机制。方法：40只SD大鼠随机分成空白对照组,急性中毒对照组,小剂量奥美拉唑治疗组（10mg/kg）和大剂量奥美拉唑治疗组（50mg/kg）。造模后计算溃疡指数,测定血浆内皮素（ET）、血清肿瘤坏死因子α（TNF-α）及胆碱酯酶活力,镜下观察胃黏膜病理改变。结果：成功建立急性胃黏膜损伤动物模型;在此基础上采用奥美拉唑治疗可改善中毒大鼠血液相关检测指标,显著改善胃黏膜溃疡指数（UI）及组织病理情况;且大剂量奥美拉唑组的疗效优于小剂量组（P〈0.05）。结论：奥美拉唑治疗能够改善大鼠口服有机磷农药中毒所致的急性胃黏膜损伤,大剂量奥美拉唑治疗的效果更明显;ET、TNF-α不但可作为急性中毒性胃黏膜损伤时早期血液检测指标,而且可作为治疗急性中毒性胃黏膜损伤效果的监测指标。     

蒲元和胃胶囊对内毒素血症大鼠急性胃粘膜病变的保护作用

目的观察蒲元和胃胶囊对大鼠内毒素血症模型胃黏膜的保护作用.方法 30只大鼠随机分为对照组及干预组.每组大鼠15只,干预组以1.0g?kg-1蒲元和胃灌胃,每日1次,对照组予等量生理盐水灌胃.7d后两组均经静脉注射内毒素建立内毒素血症模型.48h后处死动物,检测胃组织丙二醛含量,并进行胃粘膜溃疡指数评定.结果干预组胃MDA含量及指数评定明显小于对照组(P<0.05).结论在大鼠内毒素血症中蒲元和胃胶囊对胃胶囊黏膜有明显保护作用.     

CBS对酒精性胃溃疡大鼠胃粘膜血流的影响

采用激光多普勒法观察了不同剂量胶状铋剂对鼠胃粘膜血流的影响.结果提示:胶状铋剂对酒精造成的胃溃疡具有良好的保护作用.0～90min胃粘膜血流总量在20mg、40mg时明显高于对照组.但用药后15min胃粘膜血流并无增加.认为其保护机理主要是降低胃粘膜血管的通透性。     

替普瑞酮及雷贝拉唑对急性胃黏膜损伤大鼠 TFF3表达的研究

目的：研究替普瑞酮及雷贝拉唑对无水乙醇诱发大鼠急性胃黏膜病变的保护性作用及三叶草因子3（ TFF3）的表达。方法将大鼠按体重随机分为5组,分为正常对照组、模型组、替普瑞酮治疗组、雷贝拉唑治疗组、替普瑞酮联合雷贝拉唑治疗组（联合治疗组）,每组8只。用无水乙醇制备大鼠急性胃黏膜病变模型,苏木精—伊红染色观察各组大鼠胃黏膜组织病理学改变,免疫组织化学法测定各组大鼠胃黏膜TFF3的表达情况。结果与模型组比较,各药物治疗组胃黏膜溃疡指数明显减少,有显著性差异（P＜0．01）;与替普瑞酮治疗组比较,联合治疗组胃黏膜溃疡指数明显减少,有统计学意义（P＜0．05）;与雷贝拉唑治疗组比较,联合治疗组胃黏膜溃疡指数明显减少,有显著性差异（ P＜0．01）。 HE染色结果,与正常对照组比较,模型组大鼠的胃黏膜表面上皮细胞缺失,伴随大量炎症细胞浸润,肌层和浆膜被破坏;与模型组比较,雷贝拉唑、替普瑞酮治疗组及联合治疗组的大鼠胃黏膜表层上皮细胞缺失减少,黏膜腺体重现,浆膜结构较完整,且炎症细胞较少。免疫组织化学结果,与正常对照组比较,模型组及各药物治疗组胃黏膜TFF3的表达显著增多（ P＜0．05）。与雷贝拉唑组比较,联合治疗组大鼠胃溃疡周边TFF3的阳性细胞密度明显增加（P＜0．05）。结论替普瑞酮与雷贝拉唑可能通过上调 TFF3的表达改善无水乙醇所致大鼠胃黏膜组织损伤,促进胃黏膜的愈合,对大鼠急性胃黏膜病变起到保护作用。     

质子泵抑制剂的胃黏膜保护作用与环氧化酶-2表达

目的　探讨质子泵抑制剂 (PPIs)的胃黏膜保护作用与环氧化酶 2 (COX 2 )表达的关系。方法　♂SD大鼠ig给予雷巴拉唑、奥美拉唑或兰索拉唑 5 0mg·kg-1·d-1,对照组ig给予质量分数为 0 5 %羧基纤维素 5ml·kg-1·d-1,连续 2wk。Westernblot和免疫组化检测胃黏膜COX 2表达。酶免疫方法测定胃黏膜中前列腺素E2 (PGE2 )水平 ,评价兰索拉唑和特异性COX 2抑制剂NS 3 98对乙醇所致大鼠胃黏膜损伤的影响。结果　 3种PPI均增加大鼠胃黏膜COX 2的表达。兰索拉唑呈剂量依赖性地增加胃黏膜中PGE2 含量 ,有效地减轻乙醇对胃黏膜的损伤作用。NS 3 98有效地阻断了兰索拉唑诱导的PGE2 合成及胃黏膜保护作用。结论　PPIs通过诱导胃黏膜COX 2表达 ,增加PGE2 合成而发挥胃黏膜保护作用     

Effect of gefarnate on acute gastric mucosal lesion progression in rats treated with compound 48/80, a mast cell degranulator, in comparison with that of teprenone

We have reported that teprenone (geranylgeranylacetone), an anti-ulcer drug, prevents acute gastric mucosal lesion progression in rats treated once with compound 48/80 (C48/80), a mast cell degranulator, possibly by suppressing mucus depletion, neutrophil infiltration, and oxidative stress in the gastric mucosa. Herein, we examined the preventive effect of gefarnate (geranyl farnesylacetate), an anti-ulcer drug, on acute gastric mucosal lesion progression in rats treated once with C48/80 (0.75 mg/kg, i.p.) in comparison with that of teprenone, because the chemical structure and anti-ulcer action of gefarnate are similar to those of teprenone. Gefarnate (50, 100 or 200 mg/kg) administered orally at 0.5 h after C48/80 treatment, at which time gastric mucosal lesions appeared, reduced progressive gastric mucosal lesions at 3 h dose-dependently. At 3 h after C48/80 treatment, the gastric mucosa had decreased adherent mucus and hexosamine contents and increased myeloperoxdiase (an index of neutrophil infiltration) and xanthine oxidase activities and thiobarbituric acid reactive substances (an index of lipid peroxidation) content. Post-administered gefarnate attenuated all these changes dose-dependently. These preventive effects of gefarnate were similar to those of teprenone at a dose of 200 mg/kg. Post-administered gefarnate did not affect the increases in serum serotonin and histamine concentrations and the decrease in gastric mucosal blood flow at 3 h after C48/80 treatment like teprenone. These results indicate that orally administered gefarnate prevents acute gastric mucosal lesion progression in C48/80-treated rats possibly by suppressing mucus depletion, neutrophil infiltration, and oxidative stress in the gastric mucosa like teprenone.     

Role of central and peripheral ghrelin in the mechanism of gastric mucosal defence

Ghrelin, identified in the gastric mucosa, has been involved in the control of food intake and growth hormone (GH) release, but whether this hormone influences the gastric secretion and gastric mucosal integrity has been little elucidated. We compared the effects of intraperitoneal (i.p.) and intracerebroventricular (i.c.v.) administration of ghrelin on gastric secretion and gastric lesions induced in rats by 75% ethanol or 3.5 h of water immersion and restraint stress (WRS) with or without suppression of nitric oxide (NO)-synthase or functional ablation of afferent sensory nerves by capsaicin. The number and the area of gastric lesions was measured by planimetry, the GBF was assessed by the H₂-gas clearance method and blood was withdrawn for the determination of the plasma ghrelin and gastrin levels. In addition, the gastric mucosal expression of mRNA for CGRP, the most potent neuropeptide released from the sensory afferent nerves, was analyzed in rats exposed to WRS with or without ghrelin pre-treatment. Ghrelin (5–80 μg/kg i.p. or 0.6–5 μg/kg i.c.v.) increased gastric acid secretion and attenuated gastric lesions induced by ethanol and WRS. This protective effect was accompanied by a significant rise in the gastric mucosal blood flow (GBF), luminal NO concentration and plasma ghrelin and gastrin levels. Ghrelin-induced protection was abolished by vagotomy and significantly attenuated by L-NNA and deactivation of afferent nerves with neurotoxic dose of capsaicin. The signal for CGRP mRNA was significantly increased in gastric mucosa exposed to WRS as compared to that in the intact gastric mucosa and this was further enhanced in animals treated with ghrelin. We conclude that central and peripheral ghrelin exerts a potent protective action on the stomach of rats exposed to ethanol or WRS, and these effects depend upon vagal activity and hyperemia mediated by the NOS-NO system and CGRP released from sensory afferent nerves.     

Protective effect of coadministered superoxide dismutase and catalase against stress-induced gastric mucosal lesions

1. There are conflicting reports as to the protective effect of coadministered native superoxide dismutase (SOD) and catalase against gastric mucosal lesions in rats with water immersion restraint (WIR) stress. It is unclear how coadministered native SOD and catalase protect against WIR stress-induced gastric mucosal lesions. Therefore, in the present study, we re-examined the protective effect of coadministered native SOD and catalase against gastric mucosal lesions in rats with WIR stress. 2. Gastric mucosal lesions were induced in Wistar rats by 3 h WIR. Rats were injected subcutaneously with a mixture of purified bovine erythrocyte SOD and bovine liver catalase 1 h before the onset of WIR. Ulcer index, serum SOD, catalase and xanthine oxidase (XO), uric acid and gastric mucosal SOD, catalase, XO, myeloperoxidase (MPO; an index of tissue neutrophil infiltration), non-protein sulfhydryl (NP-SH) and thiobarbituric acid-reactive substances (TBARS; an index of lipid peroxidation) were assayed in all rats used. 3. Rats with 3 h WIR showed gastric mucosal lesions. Pre-administration of SOD plus catalase to rats with WIR prevented lesion formation. In the serum of rats with WIR alone, XO activity and uric acid concentration increased, whereas SOD and catalase activities did not change. Pre-administration of SOD plus catalase to rats with WIR did not affect increased serum XO activity and uric acid concentration, but did increase serum SOD and catalase activities. In the gastric mucosa of rats with WIR alone, increases in MPO activity and TBARS concentration and a decrease in NP-SH concentration occurred, whereas XO, SOD and catalase activities did not change. Pre-administration of SOD plus catalase to rats with WIR attenuated the changes in gastric mucosal MPO activity and TBARS and NP-SH concentrations, but did not affect gastric mucosal XO, SOD and catalase activities. Pre-administration of SOD plus catalase (in an inactivated form) to rats with WIR had no effect on gastric mucosal lesion formation and the levels of serum and gastric mucosal parameters studied. 4. These results indicate that coadministered native SOD and catalase protect against gastric mucosal lesions in rats with WIR stress and suggest that this protective effect of coadministered native SOD and catalase could be due to their activity to scavenge XO-derived active oxygen species that are increased in the blood.