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.     

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。     

瑞巴派特对双抗致大鼠胃黏膜损伤的保护作用及机制

目的探讨瑞巴派特对阿司匹林联合氯吡格雷(双抗)引起的胃黏膜损伤的影响及机制。方法将30只雄性SD大鼠随机分为对照组、双抗损伤组和瑞巴派特保护组。双抗损伤组大鼠给予阿司匹林(10.41 mg·kg~(-1)·d~(-1))联合氯吡格雷(7.81 mg·kg~(-1)·d~(-1))灌胃,瑞巴派特保护组大鼠在每次行双抗灌胃前1 h用瑞巴派特100 mg·kg~(-1)·d~(-1))对大鼠进行灌胃预处理,对照组给予等量的生理盐水灌胃,连续14 d;实验第15天处死所有大鼠,评估胃黏膜大体及病理损伤情况,应用免疫组化法检测胃黏膜中VEGF的表达,应用Western blotting检测胃黏膜中EGF的表达,应用TUNEL法检测胃黏膜中细胞的凋亡。结果与对照组相比,双抗损伤组大鼠胃黏膜大体及病理损伤明显增加,胃黏膜中EGF、VEGF表达明显减少(P0.05),胃黏膜细胞凋亡显著增加(P0.05);与双抗损伤组相比,瑞巴派特保护组胃黏膜损伤明显减轻,胃黏膜中EGF、VEGF表达明显增加(P0.05),胃黏膜细胞凋亡显著降低(P0.05)。结论瑞巴派特对双抗引起的胃黏膜损伤有一定的保护作用,其机制可能通过增加胃黏膜中EGF、VEGF的表达、降低细胞凋亡而促进损伤黏膜的修复。     

瑞巴派特对氯吡格雷所致人胃黏膜上皮细胞损伤的保护作用及其机制研究

背景:长期服用氯吡格雷可引起胃肠道损伤。瑞巴派特是一种新型胃黏膜保护剂,其用于防治氯吡格雷相关胃黏膜损伤的疗效尚不明确。目的:探讨瑞巴派特对氯吡格雷所致人胃黏膜上皮细胞损伤的保护作用及其可能机制。方法:以氯吡格雷处理的人胃黏膜上皮细胞株GES-1作为氯吡格雷组,以氯吡格雷联合不同浓度(0.2、0.5、1.0 mmol/L)瑞巴派特预处理的GES-1细胞作为瑞巴派特组,同时设立阴性对照组。采用MTT法检测细胞增殖抑制情况;采用倒置相差显微镜观察细胞形态学变化;采用蛋白质印迹法检测三叶因子1(TFF1)、磷酸化细胞外信号调节激酶1/2(p-ERK1/2)表达。结果:MTT法检测结果显示,瑞巴派特0.2、0.5、1.0 mmol/L组GES-1细胞增殖抑制率均显著低于氯吡格雷组(P<0.05)。倒置相差显微镜观察发现,氯吡格雷可诱导GES-1细胞损伤,而瑞巴派特可减轻氯吡格雷所致的细胞损伤。蛋白质印迹法检测结果显示,氯吡格雷组GES-1细胞TFF1蛋白表达较阴性对照组显著升高(P<0.05);瑞巴派特0.2、0.5、1.0 mmol/L组TFF1蛋白表达均较氯吡格雷组进一步升高,且作用呈浓度依赖性(P<0.05)。氯吡格雷组GES-1细胞p-ERK1/2蛋白表达较阴性对照组显著升高(P<0.05);瑞巴派特0.2、0.5、1.0 mmol/L组p-ERK1/2蛋白表达均较氯吡格雷组显著降低,作用亦呈浓度依赖性(P<0.05)。结论:瑞巴派特可能通过抑制ERK信号通路上调TFF1蛋白表达,从而参与调控氯吡格雷所致GES-1细胞损伤的修复,此过程是瑞巴派特防治氯吡格雷相关胃黏膜损伤的可能机制之一。     

瑞巴派特灌肠治疗溃疡性结肠炎的疗效及其机制

目的探讨瑞巴派特灌肠治疗溃疡性结肠炎的疗效及机理。方法42例溃疡性结肠炎患者随机分为治疗组和对照组各21例。治疗组采用瑞巴派特＋强的松＋黄连素灌肠治疗,对照组采用柳氮磺胺吡啶＋强的松＋黄连素灌肠治疗,两组均治疗4周。治疗前后测定血清IL-8和IL-10水平。结果治疗组总有效率明显高于对照组（P〈0.05）;治疗组治疗后血清IL-8水平明显降低,IL-10明显升高,与对照组比较有统计学差异（P〈0.05或〈0.01）。结论瑞巴派特灌肠治疗溃疡性结肠炎有明显疗效,其治疗作用与改善患者细胞炎症因子平衡有关。     

瑞巴派特对提高胃溃疡愈合质量的实验研究

目的 比较瑞巴派特、奥美拉唑及两种药物联合应用干预大鼠胃溃疡愈合质量.方法 建立大鼠胃溃疡模型40只,均分为对照、瑞巴派特、奥美拉唑和瑞巴派特联合奥美拉唑组,7 d后观察大鼠胃溃疡大体形态,超声探察溃疡胃壁全层结构,局部组织学形态及检测黏膜白细胞介素(IL)-8,前列腺素(PG)E2和丙二醛(MDA)含量.结果 ①超声探查显示,对照组溃疡指数为(22.3±1.8)mm2,瑞巴派特组为(9.2±1.0)mm2,奥美拉唑组为(9.8±1.3)mm2,联合治疗组为(4.8±1.2)mm2.对照组均比用药组高(P值均＜0.05),瑞巴派特组和奥美拉唑组均比对照组降低(P值均＜0.05).②离体组织超声探查显示,对照组胃壁厚度明显增加、层次结构模糊消失,用药组胃壁厚度部分恢复正常、胃壁各层次结构部分重建.③组织学表现,用药组溃疡侵袭范围、炎性细胞浸润程度均明显轻于对照组,且周边黏膜再生程度明显优于对照组.④对照组胃黏膜IL-8为(1387.8±132.6)pg/ml,瑞巴派特组为(970.0±91.6)pg/ml,奥美拉唑组为(1102.2±76.9)pg/ml,联合治疗组为(934.4±110.2)pg/ml.对照组均比各用药组高(P值均＜0.05),瑞巴派特组与联合治疗组比奥美拉唑组明显降低(P值均＜0.05).⑤对照组胃黏膜MDA为(13.0±2.6)nmol/ml.瑞巴派特组为(8.5±4.8)nmol/ml,奥美拉唑组为(9.4±1.4)nmol/ml,联合治疗组为(4.6±1.4)nmol/ml.奥美拉唑组与瑞巴派特组均明显高于联合治疗组,且低于对照组(P值均＜0.05).⑥对照组胃黏膜PGE2为(55.0±22.5)pg/ml,瑞巴派特组为(103.5±12.5)pg/ml,奥美拉唑组为(96.9±7.0)pg/ml,联合治疗组为(235.5±26.0)pg/ml.奥美拉唑组与瑞巴派特组均明显高于对照组·且低于联合治疗组(P值均＜0.05).结论 与奥美拉唑相比,瑞巴派特同样能促进溃疡愈合进程,提高溃疡愈合质量;联合应用奥美拉唑,以不同机制同时作用于溃疡愈合过程,能更好地兼顾溃疡愈合的速度和质量.     

瑞巴派特通过抑制miR-877-5p的表达减轻阿司匹林对人胃黏膜上皮细胞损伤的研究

目的研究瑞巴派特是否通过抑制miR-877-5p的表达减轻阿司匹林对人胃黏膜上皮细胞GES-1的损伤。方法体外培养GES-1细胞株,将其分为空白对照组、阿司匹林(IC10浓度)损伤组和阿司匹林(IC10浓度)联合不同浓度瑞巴派特(0.2、0.5、1.0 mmol/L)保护组,利用qRT-PCR检测miR-877-5p的表达情况。转染miR-877-5p inhibitors到阿司匹林损伤组的细胞,转染miR-877-5p mimics到0.5 mmol/L瑞巴派特保护组的细胞,CCK-8法检测细胞增殖情况,流式细胞技术检测细胞凋亡情况。利用miRNA靶基因数据库预测miR-877-5p的靶基因,并利用生物信息学分析miR-877-5p的功能。结果阿司匹林损伤组中的miR-877-5p表达量明显高于瑞巴派特保护组(P0.05),miR-877-5p表达量在保护组中随着瑞巴派特浓度增加而逐渐降低(F=71.87,P0.05)。转染miR-877-5p inhibitors能减轻阿司匹林对人胃黏膜上皮细胞增殖的抑制作用(P0.05),抑制细胞的凋亡(P0.05)。转染miR-877-5p mimics能抑制瑞巴派特对细胞的增殖效应(P0.05),促进细胞凋亡(P0.05)。生物信息学发现,miR-877-5p共有945个靶基因,这些靶基因多参与c AMP信号通路、MAPK信号通路、PI3K-Akt信号通路等发挥作用。结论瑞巴派特通过抑制miR-877-5p的表达,减轻阿司匹林对人胃黏膜上皮细胞GES-1的损伤。     

瑞巴派特和埃索美拉唑防治非甾体抗炎药胃病的疗效对比

[目的]观察对比瑞巴派特和埃索美拉唑防治长期服用非甾体抗炎药（NSAIDs）所致胃肠黏膜损伤的临床疗效.[方法]对160例服用NSAIDs患者,随机分为A、B、C组.A组60例单用NSAIDs,B组50例加服瑞巴派特,C组50例加服埃索美拉唑,8～12周后进行症状随访及胃镜检查.[结果]3组间在临床症状、胃黏膜急性糜烂、消化性溃疡及病情程度等方面比较差异均有统计学意义（P＜0.05）.在具有溃疡危险因素的患者中,C组防治效果优于B组,B组又优于A组,3组间差异有统计学意义（P＜0.05）.[结论]瑞巴派特和埃索美拉唑能有效防治NSAIDs胃病发生,具有溃疡危险因素的患者应同时服用埃索美拉唑,普通患者服用瑞巴派特即可达到防治目的.     

电针足三里穴抗大鼠应激性胃黏膜损伤的作用途径

[目的]探讨电针（EA）足三里穴抗大鼠应激性胃黏膜损伤的作用途径。[方法]采用束缚-冷应激方法制备大鼠应激性胃溃疡模型，观察切断膈下迷走神经或切除腹腔交感神经节及注射受体阻断剂对EA抗应激性胃黏膜损伤的影响。[结果]EA-模型组胃黏膜损伤明显减轻，溃疡指数（UI）与模型组比较差异有统计学意义（P〈0．01）。切断双侧膈下迷走神经或切断腹腔交感神经节，大鼠UI减小，分别与腹部假手术组比较差异有统计学意义（P〈0．01）。静脉给予β受体阻断剂普萘洛尔，可部分削弱EA对胃黏膜损伤的保护作用，与0．85％氯化钠组比较P〈0．01；而给予M受体阻断剂阿托品、α受体阻断剂酚妥拉明对EA保护胃黏膜损伤作用无明显影响（P〉0．05）。[结论]迷走神经和交感神经参与了电针对应激性胃黏膜损伤的调控作用，其作用部分是由β受体介导实现的。     

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。     

Mitigation of indomethacin-induced gastric mucosal lesions by a potent specific type V phosphodiesterase inhibitor

AIM: To investigate the gastroprotective effect of vardenafil against indomethacin-induced gastric damage.METHODS: Forty-eight female Wistar albino rats were randomly divided into 6 groups. Group 1 received saline only. Group 2 (indomethacin) received indomethacin.Rats in group 3 and 4 were pretreated with different doses of famotidine. Group 5 and 6 were pretreated with different doses of vardenafil. Rats in groups 3 to 6 received 25 mg/kg indomethacin 30 min after pretreatment. The animals were sacrificed 6 h later and their stomachs were opened. Gastric lesions were counted and measured. The stomach of each animal was divided in two parts for histopathological examinations and nitric oxide (NO) and malondialdehyde (MDA) assays, respectively.RESULTS: There were no gastric mucosal lesion in the saline group but all rats in the indomethacin group had gastric mucosal ulcerations (ulcer count; 6.25 ± 3.49,and mean ulcer area; 21.00 ± 12.35). Ulcer counts were diminished with famotidine 5 mg/kg (4.12 ± 2.47, P > 0.05), 20 mg/kg (2.37 ± 4.43, P < 0.05), vardenafil 2 mg/kg (4.37 ± 3.06), and vardenafil 10 mg/kg (1.25 ± 1.38, P < 0.05) compared to the indomethacin group.Gastric mucosal lesion areas were diminished with famotidine 5 mg/kg (8.62 ± 2.97, P < 0.001), famotidine 20 mg/kg (0.94 ± 2.06, P < 0.001), vardenafil 2 mg/kg (6.62 ± 5.87, P < 0.001), and vardenafil 10 mg/kg (0.75 ± 0.88, P < 0.001) compared to the indomethacin group. MDA levels were significantly higher in indomethacin group (28.48 ± 14.51), compared to the famotidine 5 mg/kg (6,21 ± 1.88, P < 0.05), famotidine 20 mg/kg (5.88 ± 1.60. P < 0.05), vardenafil 2 mg/kg (15.87 ± 3.93, P < 0.05), and vardenafil 10 mg/kg (10.97 ± 4.50,P < 0.05). NO concentration in gastric tissues of the famotidine groups were significantly increased ( P < 0.05),but the NO increases in the vardenafil groups were not statistically significant. Histopathology revealed diminished gastric damage for pretreatment groups compared to the indomethacin group ( P < 0.05).CONCLUSION: Vardenafil affords a significant dosedependent protection against indomethacin induced gastric mucosal lesions in rats.     

Rebamipide decreases the susceptibility of gastric mucosa to acid-induced injury in rats by inhibiting neutrophil activation

We previously demonstrated that activated neutrophils increased the susceptibility of gastric mucosa to acid-induced injury in rats. As rebamipide, an anti-ulcer agent, inhibits neutrophil activation, we examined whether the rebamipide reduces stress-induced gastric mucosal injury by decreasing susceptibility to acid-induced gastric mucosal injury in rats. Increase in both gastric mucosal permeability and gastric microvascular permeability evaluated by (51)Cr-EDTA clearance and Evans blue leakage, respectively, at 6 hr after Water-Immersion Restraint Stress (WIR) were significantly lower in animals with leukocytopenia than those in controls. Pretreatment with neutrophil elastase (NE) inhibitors, an anti-P-selectin monoclonal antibody (MAb), and rebamipide significantly inhibited these increases at 6 hr after WIR. These treatments also inhibited decrease in gastric mucosal blood flow observed at 6 hr after WIR. Acid-induced exacerbation of gastric mucosal injury in rats at 6 hr after WIR was inhibited by NE inhibitors, anti-P-selectin MAb, and rebamipide. Rebamipide significantly inhibited WIR-induced increase in gastric MPO activity at 8 hr after WIR. Observations in the present study raised a possibility that rebamipide decreases the susceptibility of gastric mucosa to acid-induced injury by inhibiting neutrophil activation.     

复方尿囊素片对乙醇所致大鼠胃黏膜损伤保护作用的实验研究

目的研究复方尿囊素片对乙醇所致大鼠急性胃黏膜损伤的预防保护作用及其机制。方法 60只健康雄性Wistar大鼠随机分为5组：乙醇损伤组、空白对照组、硫糖铝保护组、氢氧化铝保护组、复方尿囊素保护组。保护组分别用硫糖铝、氢氧化铝及复方尿囊素片提前给大鼠灌胃,其后用乙醇灌胃致急性胃黏膜损伤,然后分别测定各组胃黏膜溃疡指数、黏膜损伤积分、胃黏膜血流、黏膜前列腺素E2（PGE2）及一氧化氮（NO）含量,并在显微镜及电镜下观察胃黏膜组织学改变。结果复方尿囊素保护组的各项检测指标显示：溃疡指数、损伤积分显著低于乙醇损伤组（P=0.000,P=0.000）,明显低于氢氧化铝保护组（P=0.020,P=0.004）,也低于硫糖铝保护组,但差异无统计学意义（P=1.000,P=1.000）;黏膜血流值较乙醇损伤组明显增加（P=0.000）,明显高于氢氧化铝保护组（P=0.019）,与硫糖铝保护组的差异无统计学意义（P=0.266）;黏膜PGE2及NO含量均较乙醇损伤组明显增加（P=0.000,P=0.001）,明显高于氢氧化铝保护组（P=0.002,P=0.001）,也高于硫糖铝保护组,但差异无统计学意义（P=0.451,P=0.199）。结论复方尿囊素片对乙醇所致大鼠急性胃黏膜损伤有明显的预防保护作用,其作用是通过增加胃黏膜血流、增加黏膜PGE2及NO含量等机制实现的。     

Rebamipide reduces indomethacin-induced gastric injury in mice via down-regulation of ICAM-1 expression

Non-steroidal anti-inflammatory drugs (NSAIDs) induced gastric mucosal injury occurs through subsequent events following free radical production derived from activated neutrophils. In this study, we hypothesized that rebamipide, a novel anti-ulcer agent, exerts a protective effect on NSAID-induced gastric injury through its antioxidant properties. The protective effect of rebamipide in a mouse model of indomethacin-induced gastric injury and mechanisms for this effect were investigated. Pre-treatment with rebamipide significantly inhibited indomethacin-induced gastric mucosal injury in mice. Gastric thiobarbituric acid reactive substances (TBARS) levels and myeloperoxidase (MPO) activity substantially increased 3 hr after indomethacin administration. These increases were significantly inhibited by pre-treatment with rebamipide. Furthermore, rebamipide pre-treatment notably decreased intercellular adhesion molecule-1 (ICAM-1) expression that was up-regulated in gastric tissue treated with indomethacin. Therefore, rebamipide may reduce indomethacin-induced gastric mucosal injuries through its antioxidant effect, which inhibits the neutrophil activation step following up-regulation of ICAM-1 expression on endothelial cells.     

Protective effect of Irsogladine on monochloramineinduced gastric mucosallesions in rats:a comparative study with rebamipide

ＩＮＴＲＯＤＵＣＴＩＯＮＨｅｌｉｃｏｂａｃｔｅｒｐｙｌｏｒｉ,ｒｅｃｏｇｎｉｚｅｄａｓｔｈｅｍａｊｏｒｃａｕｓｅｏｆｇａｓｔｒｉｔｉｓａｎｄｐｅｐｔｉｃｕｌｃｅｒｄｉｓｅａｓｅｓ［１－３］ｈａｓａｈｉｇｈａｃｔｉｖｉｔｙｏｆｕｒｅａｓｅ,ｒｅｓｕｌｔｉｎｇｉｎａｈｉｇｈｃｏｎｃｅｎｔｒａｔｉｏｎｏｆａｍｏｎｉａ（ＮＨ４ＯＨ）ｉｎｔｈｅｓｔｏｍａｃｈｏｆｉｎｆｅｃｔｅｄｐａｔｉｅｎｔｓ［３］．ＳｉｎｃｅＨ．ｐｙｌｏｒｉａｓｓｏｃｉａｔｅｄｃｈｒｏｎｉｃａｃｔｉｖｅｇａｓｔｒｉｔｉｓｉｓｃｈａｒａ…     

Assessing the efficacy of famotidine and rebamipide in the treatment of gastric mucosal lesions in patients receiving long-term NSAID therapy (FORCE—famotidine or rebamipide in comparison by endoscopy)

Background Nonsteroidal anti-inflammatory drugs (NSAIDs) and Helicobacter pylori infection are major causes of gastric mucosal lesions. In Japan, histamine-2 receptor antagonists are frequently prescribed, but the literature regarding their efficacy is limited. In this study, we compare the effects of famotidine and rebamipide on NSAID-associated gastric mucosal lesions using upper gastrointestinal endoscopy. Methods This study examined 112 patients taking NSAIDs for either gastric hemorrhage or erosion. Before treat-ment, the patients were assessed by endoscopy. Using blind randomization, patients were divided into two groups: group F (famotidine, 20 mg/day) and group R (rebamipide, 300 mg/day). Efficacy was examined 4 weeks later using endoscopy. Results After treatment, the Lanza score decreased significantly in group F (P < 0.001) but not in group R (P = 0.478). The change in the Lanza score in group F was significantly greater (P = 0.002) than that in group R. Conclusions Famotidine was superior to rebamipide in treating NSAID-associated mucosal lesions.     

Efficacy of famotidine in patients with acute gastric mucosal injury after continuous infusion of cisplatin plus vindesine

The effect of famotidine (H₂ blocker) on the gastroduodenal mucosal injury induced by chemotherapy in non-small-cell lung cancer patients was prospectively evaluated from the clinical and endoscopic findings obtained in a randomized double-blind study. The patients, who were administered cisplatin (25 mg/m²/day, continuous infusion, days 1–5) and vindesine (3 mg/m², bolus, days 1 and 8), were randomized into two groups, those administered famotidine (40 mg/day, oral) and those administered the placebo. The patients were examined by gastroduodenoscopy within 7 days before and after chemotherapy. There were 27 patients in the famotidine group and 28 patients in the placebo group. The gastric mucosal score after chemotherapy was significantly lower in the famotidine group than in the placebo group (P<0.01), and in the 42 patients without symptoms than in the 13 patients (placebo group: 8, famotidine group: 5) with upper gastrointestinal symptoms (P<0.01). The pH of the gastric juice after the chemotherapy significantly decreased in the placebo group (P<0.05), and was significantly lower in the placebo group than in the famotidine group (P=0.01). The co-administration of famotidine was effective in the prevention and control of chemotherapy-induced gastric mucosal injury.Abbreviations NSCLC non-small-cell lung cancer - GDS gastroduodenoscopy This work was supported by a Grant in aid for Cancer Research from the Foundation for Promotion of Japanese Cancer Research     

瑞巴派特可提高胃溃疡的组织学愈合质量

背景：质子泵抑制剂的广泛应用，以及将根除幽门螺杆菌（H．pytori）感染作为治疗胃溃疡的主要手段，极大地提高了消化性溃疡的临床愈合率，但溃疡易复发的难题仍亟待解决。溃疡愈合质量，尤其是组织学愈合质量正日益受到关注。目的：观察活动性胃溃疡患者应用瑞巴派特联合法莫替丁与单用奥美拉唑治疗前后的胃黏膜组织学变化，比较两组溃疡的组织学愈合质量。方法：将110例经胃镜检查证实伴有H．pylori感染的活动性胃溃疡患者随机分为治疗组和对照组。治疗组口服瑞巴派特片和法莫替丁片，对照组口服奥美拉唑胶囊，疗程均为6周。治疗结束后。两组复查胃镜。内镜下取胃溃疡周围黏膜（相当于原取材点处）组织2～4块，观察两组治疗前后的胃黏膜组织学变化，着重从炎性细胞浸润程度、黏膜形态结构和上皮细胞内中性黏液含量三个方面观察胃黏膜组织学恢复情况。结果：治疗6周后，两组胃黏膜组织形态好转程度相似，但治疗组胃黏膜上皮细胞内中性黏液含量恢复程度较对照组显著（p=0．0039），腺体密度较治疗前显著增加（P=0．0485）。结论：无论H．pylori感染根除与否，瑞巴派特均可使胃黏膜上皮细胞内中性黏液含量和腺体密度较快恢复，增强胃黏膜上皮细胞成熟程度，提高胃黏膜防御功能，从而提高溃疡的组织学愈合质量。