马来酸伊索拉定联合三联疗法对幽门螺杆菌感染小鼠治疗作用的实验研究

目的观察马来酸伊索拉定(Irsogladine Maleate,IM)联合三联疗法对幽门螺杆菌(H.pylori)感染小鼠的根除作用其及对H.pylori所致胃黏膜炎症的修复作用。方法 60只KM小鼠随机分为6组,空白对照组、H.pylori感染模型组和4个药物治疗组。治疗组分别给予标准三联、铋剂四联、小剂量IM+标准三联及大剂量IM+标准三联药物灌胃治疗。快速尿素酶试验(RUT)联合组织病理学Giemsa染色判断H.pylori根除情况,HE染色判断胃黏膜炎症情况。结果标准三联组7例H.pylori根除成功,铋剂四联组、小剂量IM+标准三联组及大剂量IM+标准三联组均有8例根除成功,四组根除率两两比较,差异无统计学意义(P0.05)。大剂量IM+标准三联组对胃黏膜慢性炎性反应的修复作用与铋剂四联组相当,优于标准三联组,差异有统计学意义(P0.05)。结论大剂量或小剂量IM联合标准三联对H.pylori感染小鼠的H.pylori根除率与铋剂四联相当,略高于标准三联,IM联合标准三联可明显改善H.pylori感染根除后的胃黏膜慢性炎性反应,且具有剂量依赖性。     

标准三联、新四联及10天序贯疗法对幽门螺杆菌感染的疗效观察

目的观察标准三联、新四联及10天序贯疗法对幽门螺杆菌(H.pylori)感染的疗效。方法 215例H.pylori阳性的患者随机分为3组。A组72例,用新四联疗法(雷贝拉唑+可乐必妥+阿莫西林+果胶铋治疗7天);B组72例,用10天序贯疗法(奥美拉唑+阿莫西林治疗5天,继之以奥美拉唑+克拉霉素+替硝唑再治疗5天);C组71例,用标准三联疗法(奥美拉唑+阿莫西林+克拉霉素治疗7天)。治疗后,3组均继续服用3周奥美拉唑。停药4周后复查胃镜、快速尿素酶实验与14C尿素呼气试验,评估H.pylori根除率及溃疡愈合率。结果 215例均完成抗H.pylori治疗周期及随访。A、B、C三组的H.pylori根除率分别为83.33%、88.89%和81.69%;溃疡愈合率分别为86.44%、90.16%和84.91%。B组H.pylori根除率及溃疡愈合率比A、C组稍高,H.pylori根除率与A、C组比较差异亦有统计学意义(P0.05),但A、C组间H.pylori根除率比较差异无统计学意义(P0.05);三组溃疡愈合率比较差异无统计学意义(P0.05),不良反应发生率组间比较差异无统计学意义(P0.05),普遍均能耐受。结论标准三联、新四联及10天序贯疗法均能有效根除H.pylori感染,无明显不良反应,但10天序贯疗法更为理想。     

兰索拉唑三联疗法根除幽门螺杆菌的疗效及耐药研究

目的 研究以兰索拉唑为基础的不同治疗方案对幽门螺杆菌(H.pylori)根除率的影响并了解湖南地区H.pylori 耐药情况.方法 将76例H.pylori感染患者分成兰索拉唑加克拉霉素、阿莫西林组(LCA组)38例和兰索拉唑加克拉霉素与甲硝唑组(LCM组)38例,治疗1周,治疗前采用快速尿素酶试验(RUT)、14C-尿素呼气试验(14C-UBT)、组织学检查筛选,入选患者进行H.pylori培养及药物敏感性检测.治疗后停用抗生素至少4周行14C-UBT复查.结果 LCA组共有31例完成治疗,26例H.pylori 被根除, 根除率为83.87%;LCM组共有35例完成治疗,21例H.pylori 被根除, 根除率为60.00%.LCA组根除率明显高于LCM组(P＜0.05).阿莫西林、克拉霉素及甲硝唑耐药率分别为0.00%、28.00%和92.00%,对克拉霉素及甲硝唑均耐药率为24.00%;两组药物副作用发生率比较无明显差别(P＞0.05).结论 (1) 兰索拉唑联合克拉霉素、阿莫西林组较联合克拉霉素与甲硝唑组H.pylori根除率高;(2)湖南地区H.pylori对甲硝唑耐药率最高(92.00%),克拉霉素次之(28.00%).尚未发现对阿莫西林耐药的菌株.     

大剂量阿莫西林/埃索美拉唑二联方案根除幽门螺杆菌

目的评估大剂量阿莫西林/埃索美拉唑二联方案在幽门螺杆菌(Helicobacter pylori,H.pylori)感染初次治疗患者中的疗效及安全性.方法 142例H.pylori感染的初次治疗患者随机进入大剂量阿莫西林/埃索美拉唑二联方案(EA)组(埃索美拉唑20 mg qid+阿莫西林0.75g qid,疗程14d)和铋剂四联方案(EBAC)组(埃索美拉唑20mg bid+枸橼酸铋钾220 mg bid+阿莫西林1.0g bid+克拉霉素0.5g bid,疗程14d),治疗结束后6wk复查尿素呼气试验,判断H.pylori根除疗效.结果共131例患者完成研究,EA组按意向治疗(intentionto-treat,ITT)与按方案(per-protocol,PP)分析H.pylori根除率分别为82.9%和89.2%,EBAC组分别为86.1%和93.9%,两组根除率的ITT、PP分析差异均无统计学意义(P0.05).按PP分析,EBAC组不良反应发生率明显高于EA组(15.2%vs 3.1%,P0.05).结论大剂量阿莫西林/埃索美拉唑二联方案可作为安全、有效的H.pylori感染初次治疗方案.     

含替硝唑序贯疗法根除幽门螺杆菌62例

目的: 观察由泮托拉唑、替硝唑、阿莫西林、克拉霉素组成的10日序贯疗法根除幽门螺杆菌( H pylori)的疗效.方法: 将经胃镜检查确诊为慢性胃炎和消化性溃疡且H pylori阳性的患者120例随机分为两组, 治疗组(62例)方案为前5 d给予泮托拉唑+阿莫西林, 后5 d给予泮托拉唑+克拉霉素+替硝唑;对照组(58例)三联疗法为泮托拉唑+阿莫西林+克拉霉素, 疗程7 d. 比较治疗后两组患者H pylori根除率.结果: 治疗组和对照组H pylori ITT根除率分别为83.87%和67.24%, PP根除率分别为89.66%和72.22%, 两组分别有统计学意义( P<0.05).结论: 含替硝唑的10日序贯疗法治疗H pylori感染具有较高的根除率.     

含铋剂四联疗法根除消化性溃疡幽门螺杆菌感染的疗效

目的:探讨含铋剂的四联疗法在根除幽门螺杆菌(Helicobacter pylori,H.pylori)感染的疗效研究.方法:将H.pylori感染的消化性溃疡病例288例,随机分为观察组和对照组各144例;观察组:胶体果胶铋+泮托拉唑+呋喃唑酮+阿莫西林四联疗法,疗程10 d;对照组:泮托拉唑+阿莫西林+克拉霉素标准三联疗法,疗程10 d.将两组溃疡总有效率、H.pylori根除率和不良反应进行比较.结果:观察组较对照组有较高的根除率,观察组分别为胃溃疡91.5%、十二指肠溃疡94.1%,对照组则分别为73.5%、71.1%,差异有统计学意义(P0.05).药物不良反应发生率差异无统计学意义(P0.05).结论:含铋剂四联疗法根除H.pylori感染根除率高、价廉,潜在的不良反应发生率低,是目前较为理想的根除H.pylori方案.     

重组人乳铁蛋白对幽门螺旋杆菌胃炎小鼠空泡毒素蛋白A、肿瘤坏死因子α含量的影响

目的:本研究探讨重组人乳铁蛋白(recombinant human lactoferrin,rhLF)联合三联疗法是否能够提高小鼠胃幽门螺旋杆菌(Helicobacter pylori,H.pylori)根除率,能否降低小鼠胃黏膜炎症反应,初步揭示rhLF对H.pylori感染小鼠胃黏膜炎症的作用特点及相关机制.方法:192只Babl/c小鼠用H.pylori ATCC43504感染建立胃炎模型,随机分为A组(标准三联+rhLF)、B组(rhLF)、C组(标准三联)、D组(生理盐水),小鼠胃黏膜采用特殊银染评定H.pylori定植情况、HE染色镜检炎症积分值,采用ELISA试剂盒测定胃组织匀浆肿瘤坏死因子(tumor necrosis factor,TNF)-α含量.并通过RT-PCR方法检测各组药物对H.pyloriATCC43504的主要致病因子空泡毒素蛋白(vacuolating cytotoxin,VacA)mRNA表达水平.数据均有SPSS17.0软件分析.结果:与D组比较,A、B、C组小鼠胃黏膜特殊银染色镜检H.pylori定植率、HE染色镜检胃黏膜炎症积分明显降低(P0.05);与B、C组比较,A组小鼠胃黏膜特殊银染色镜检H.pylori定植、HE染色镜检胃黏膜炎症积分明显降低(P0.05);A、B、C、D组胃组织匀浆中体内TNF-α含量分别为28.64pg/mL±12.07 pg/mL、300.16 pg/mL±59.10pg/mL、54.96 pg/mL±15.02 pg/mL、503.25pg/mL±1.35 pg/mL;rhLF联合三联疗法可降低胃组织匀浆液中TNF-α含量(P0.01),与生理盐水组、标准三联组、rhLF组比较差异有统计意义.rhLF联合三联疗法可降低胃组织匀浆液中VacA mRNA表达水平(P0.01),与生理盐水组、标准三联组、rhLF组比较差异有统计意义.结论:RhLF联合三联疗法能够提高H.pylori根除率;降低胃黏膜炎症反应,此作用可能与rhLF联合三联疗法能够降低促炎症因子释放有关.rhLF可有效抑制VacA mRNA表达,提示rhLF具有下调H.pylori毒性的潜在作用.     

根除幽门螺杆菌对功能性消化不良疗效的研究

背景:功能性消化不良(FD)的患病率始终居高不下,目前就幽门螺杆菌(H.pylori)阳性的FD患者是否需根除H.pylori尚存在争议。目的:探讨根除H.pylori对H.pylori阳性FD患者的疗效。方法:200例H.pylori阳性FD患者随机分为治疗组(100例.予以枸橼酸铋雷尼替丁400mg+阿莫西林1000mg+克拉霉素250mg,2次/d,疗程1周)和对照组(100例,予以铝碳酸镁1000mg,3次/d,疗程1周)。随访结束后评估H.pylori根除率和FD症状改善情况。结果:治疗组的H.pylori根除率分别为87.5%(PP分析)和84.0%(ITT分析),对照组H.pylori根除率为0%。H.pylori根除亚组FD症状改善的总有效率显著高于H.pylori未根除亚组和对照组(90.5%对41.7%和45.9%,P0.01)。结论:部分H.pylori阳性FD患者根除H.pylori后,其症状可长期缓解,因此对部分H.pylori阳性FD患者根除H.pylori是一种值得推广的有效治疗手段。     

荆花胃康胶丸对小鼠体内H.pylori的根除作用及对胃黏膜上皮细胞形态的影响

[目的]观察荆花胃康胶丸对幽门螺杆菌(H.pylori)感染小鼠的体内杀菌作用及对胃黏膜上皮细胞超微形态的影响。[方法]55只SPF级KM小鼠采用短期免疫抑制联合经口感染方法建立H.pylori感染模型,随机分为空白对照组、模型对照组、荆花胃康组、三联组、联合给药组。荆花胃康组给予荆花胃康挥发油4周;三联组给予兰索拉唑、甲硝唑、克拉霉素1周;联合治疗组给予三联+荆花胃康1周后,单独继续给予荆花胃康3周;模型对照组给予灭菌注射用水;空白对照组不予干预。所有动物均于给药4周后处死,通过快速尿素酶试验、Warthin-Starry染色判断H.pylori根除率,扫描电镜下观察胃黏膜上皮细胞超微形态。[结果]荆花胃康组H.pylori根除率为4/10,三联组7/10,联合给药组8/10,差异无统计学意义;联合给药组胃黏膜上皮细胞形态最优,达到与空白对照组相当的水平,三联组次之,荆花胃康组效应最弱。[结论]荆花胃康胶丸具有小鼠体内根除H.pylori的作用,其与三联疗法联合可有效促进胃黏膜上皮细胞形态结构的恢复。     

兰索拉唑联合克拉霉素缓释胶囊阿莫西林胶囊三联治疗幽门螺杆菌疗效观察

目的兰索拉唑联合克拉霉素缓释胶囊阿莫西林胶囊三联治疗幽门螺杆菌(Helicobacter pylori,H.pylori)疗效观察。方法采用14C-尿素呼气试验阳性患者随机分为两组,观察组37例使用兰索拉唑片30 mg bid联合克拉霉素缓释胶囊250 mg bid、阿莫西林胶囊1 000 mg bid,对照组25例使用雷尼替丁胶囊150 mg bid联合甲硝唑片400 mg bid、阿莫西林胶囊1 000 mg bid:;连续服药2周,停药4周后,复测病人H.pylori、CPM变化及不良反应。结果观察组有效率100%,根除率91.89%;对照组有效率84.00%,根除率60.00%,观察组根除率高于对照组,两组比较差异有显著性(P0.05)。结论兰索拉唑联合克拉霉素缓释胶囊阿莫西林胶囊三联治疗H.pylori是有效安全的方法。     

幽门螺杆菌长期感染诱发C57B L/6小鼠胃癌模型的建立及对血管新生的影响

目的:研究H.pylori长期感染C57BL/6小鼠致胃黏膜病变及其致癌性,并从血管新生的角度探讨H.pylori感染致胃癌发生的可能机制.方法:将80只SPF级C57BL/6小鼠随机分为正常组和模型组,每组40只.正常组正常饲养,模型组经口直接灌服H.pylori标准株SS1,距末次灌胃后10 wk、25 wk、45 wk、72 wk分4批处死,每批每组各处死10只小鼠.快速尿素酶试验、Giemsa染色法观察H.pylori在胃黏膜的定植情况,HE染色观察小鼠胃黏膜病理变化,免疫组织化学法观察微血管密度(microvessel density,MVD)的变化.结果:正常组动物的胃窦、胃体及十二指肠黏膜的尿素酶实验、Giemsa染色结果均呈阴性,在末次接种H.pylori后第10周、第25周、第45周、第72周,模型组H.pylori的定植率分别为88.9%、100%、100%、100%;72 wk时,模型组慢性胃炎、萎缩性胃炎、肠化生、异型增生和胃癌的发生率分别为100%,88.9%,77.8%,33.3%和22.2%,胃黏膜组织中MVD为18.56±2.62,较正常组(2.50±1.54)明显升高(P<0.01).结论:成功建立了H.pylori长期感染诱发C57BL/6小鼠胃癌模型,且H.pylori可增加小鼠胃黏膜MVD,可能在胃黏膜的癌变中发挥作用.     

嗜酸乳杆菌预防和治疗C57BL/6小鼠幽门螺杆菌感染的实验研究

2004

In Vitro and In Vivo Inhibition of Helicobacter pylori by Lactobacillus casei Strain Shirota 2004

Lactobacillus johnsonii Lal attenuates Helicobacter pyloriassociated gastritis and reduces levels of proinflammatory chemakines in C57BL/6 mice 2005

嗜酸乳杆菌对不同毒力亚型幽门螺杆菌的体外抑制效应及作用机制 2009

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幽门螺杆菌感染诱导C57BL/6小鼠动脉硬化的病理损伤及其在粥样斑块组织中的DNA分析

目的 建立幽门螺杆菌(HP)感染的C57BL/6小鼠动脉粥样硬化模型,探讨HP感染在动脉粥样硬化发病机制中的作用.方法 将48只C57BL/6小鼠随机分为4组,即HP灌饲联合高脂饮食组、单纯HP灌饲组、单纯高脂饮食组以及生理盐水对照组,每组12只小鼠.52周后观察4组小鼠主动脉粥样硬化发生率及其病理损伤程度、胃黏膜病理特征、血脂水平,并以PCR方法检测小鼠主动脉中HP尿素酶A(ureaseA,ureA)、尿素酶C(ureaseC,ureC)、细胞毒素相关基因A(cytotoxin-associated gene A,cagA)、空泡毒素A(vacuolating cytotoxin A,vacA)的DNA表达.结果 (1)单纯HP灌饲组和生理盐水对照组无动脉粥样硬化发生,而HP灌饲联合高脂饮食组和单纯高脂饮食组动脉粥样硬化发生率高达100%和91.6%,两组问差异无统计学意义.(2)HP灌饲联合高脂饮食组、单纯HP灌饲组、单纯高脂饮食组的总胆固醇(TC)、低密度脂蛋白(LDL)和甘油三酯(TG)水平高于生理盐水对照组(P均<0.05),而高密度脂蛋白(HDL)水平低于生理盐水对照组(P均<0.05).且HP灌饲联合高脂饮食组的TC、LDL和TG水平高于单纯高脂饮食组,HDL水平低于单纯高脂饮食组,组间差异有统计学意义,P均<0.05.(3)HP灌饲联合高脂饮食组Roberts & Thompson评分总分和斑块中泡沫细胞最多数目均高于单纯高脂饮食组,P均<0.05.(4)12只HP灌饲联合高脂饮食组的小鼠动脉组织中有5例ureC检测出阳性,但未检测出ureA、cagA和vacA DNA.同时在其他3组小鼠动脉组织中均未检出HP的DNA表达.结论 给C57BL/6小鼠灌饲HP可加重高脂饮食诱发的血脂代谢紊乱和动脉粥样硬化病理损伤程度,同时在HP感染的小鼠动脉粥样硬化组织中可检出HP的ureC DNA,提示HP感染与动脉粥样硬化的发生发展可能相关.     

小鼠模型中蔓越莓汁防治幽门螺杆菌感染的实验研究

背景:根除幽门螺杆菌(H.pylori)感染有助于消化性溃疡和胃黏膜炎症的愈合,蔓越莓汁已被证实可预防尿路感染的复发。目的:探讨蔓越莓汁是否能根除或预防H.pylori感染。方法:治疗实验中,以H.pylori感染C57BL/6小鼠。感染后2周,80只小鼠随机分为4组,每组20只。A组:经口灌胃予蔓越莓汁(0.5 ml/只,1次/d)共30天;B组:三联疗法(阿莫西林50 mg/kg、枸橼酸铋6.15 mg/kg和甲硝唑22.5 mg/kg,1次/d)共14天;C组:蔓越莓汁加三联疗法:对照组:H.pylori感染后不予任何治疗。治疗实验结束后24 h和4周,各组分别处死10只小鼠,用快速尿素酶试验、细菌培养和组织病理学方法检测H.pylori感染情况。预防实验中,40只小鼠经口灌胃予蔓越莓汁(0.5 ml/只,1次/d)共25天,第26～30天时将小鼠随机分为4组,每组10只。在第26、28和30天,A组:不给予蔓越莓汁,而予H.pylori攻击3次;B组:先将H. pylori在蔓越莓汁中孵育30 min,然后再攻击小鼠;C组:给予蔓越莓汁后6 h予H. pylori攻击;对照组:不给予蔓越莓汁而仅予H. pylori攻击。在第27和29天,各组仍给予蔓越莓汁。预防实验结束后2周处死小鼠检测H. pylori感染情况。结果:治疗实验结束后24 h,A、B、C组的H. pylori清除率分别为80％、100％和90％,均显著高于对照组(P<0.01);治疗实验结束后4周,A组     

Low-dose rabeprazole, amoxicillin and metronidazole triple therapy for the treatment of Helicobacter pylori infection in Chinese patients

BACKGROUND: Rabeprazole in combination with amoxicillin and metronidazole (RAM) has been shown to be an effective second-line treatment of Helicobacter pylori infection. The effects were compared of 7-day low-dose and high dose rabeprazole in RAM for the primary treatment of H. pylori infection in Chinese patients. METHODS: Helicobacter pylori-positive dyspeptic patients were randomized to receive either (i) rabeprazole 10 mg, amoxicillin 1000 mg and metronidazole 400 mg (RAM-10) or (ii) high-dose rabeprazole 20 mg, amoxicillin 1000 mg and metronidazole 400 mg (RAM-20), each given twice daily for 7 days. Helicobacter pylori eradication was confirmed by (13)c-urea breath test 5 weeks after stopping medications. side-effects of treatments were documented. RESULTS: A total of 120 patients were eligible for analysis. By intention-to-treat and per-protocol analysis, the eradication rates were 83% and 86% in the RAM-10 group and 75% and 76% in the RAM-20 group, respectively (P = 0.26 and P = 0.17). Both regimens were well-tolerated and compliance was >98% in both groups. CONCLUSIONS: Low-dose rabeprazole in combination with amoxicillin and metronidazole is an effective, economical and well-tolerated therapy for the treatment of H. pylori infection in Chinese population.     

Enhanced plasma ghrelin levels in Helicobacterpylori-colonized,intedeukin-1-receptor type 1-homozygous knockout （IL-1R1^-/-） mice

AIM: Ghrelin is an endogenous ligand for the growth hormone secretagogue receptor, and it plays a role in stimulating the growth hormone secretion, food intake, body weight gain and gastric motility. Eradication of Helicobacter pylori (H pylori) was shown to be associated with increase of the body weight. On the other hand, H pylori infection evokes the release of gastric IL-1beta. The present study was designed to investigate the involvement of the gastric IL-1 signal in the ghrelin dynamics in H pylori-colonized mice. METHODS: Twelve-week-old female IL-1-receptor type 1-homozygous-knockout mice (IL-1R1(-/-)) and their wild-type littermates (WT) were orally inoculated with H pylori (Hp group), while other cohorts received oral inoculation of culture medium (Cont group). Thirteen weeks after the inoculation, the mice were examined. The plasma and stomach ghrelin levels and the gastric preproghrelin mRNA were measured. RESULTS: Although the WT mice with H pylori infection showed a significantly decreased body weight as compared with that of the animals without H pylori infection, H pylori infection did not influence the body weight of the IL-1R1-knockout (IL-1R1(-/-)) mice. In the H pylori-infected IL-1R1(-/-) mice, the total and active ghrelin levels in the plasma were significantly increased, and the gastric ghrelin level was decreased. No significant differences were noted in the gastric preproghrelin mRNA expression. CONCLUSION: Ghrelin secretion triggered by H pylori infection might be suppressed by IL-1beta, the release of which is also induced by the infection, resulting in the body weight loss of mice with H pylori infection.     

Ethanol intake preceding Helicobacter pylori inoculation promotes gastric mucosal inflammation in Mongolian gerbils

BACKGROUND: Mongolian gerbils have been reported to be a suitable model for Helicobacter pylori-associated gastric mucosal injury, including gastric cancer. Although ethanol is known to be one of the harmful substances in the gastric mucosa, the relationship between ethanol and H. pylori infection remains unknown. The aim of the present study is to investigate the effect of ethanol treatment prior to H. pylori inoculation on associated gastric mucosal injury. METHODS: Male Mongolian gerbils were used for the study. Helicobacter pylori was orally inoculated after 15 h fasting (Hp group). Thirty minutes prior to H. pylori inoculation, a group of gerbils was orally treated with 40% ethanol (20 mL/kg; E + Hp group). Another group of animals was treated either with H. pylori culture media alone (controls) or with 40% ethanol plus culture media (E group). Gerbils were killed 2, 4 or 12 weeks after H. pylori inoculation. Helicobacter pylori infection was confirmed by both histological examination and serological tests. Mucosal damage was evaluated histologically according to the modified Sydney system. RESULTS: Although in the controls and E group no significant change to the gastric mucose was observed, persistent H. pylori infection was seen in the mucosa and mucosal leucocyte infiltration and severe epithelial damage was observed in the Hp and E + Hp groups after 4 weeks. The histological scores for polymorphonuclear cell infiltration and myeloperoxidase activity were higher in the E + Hp group at 4 weeks than in the Hp group (P < 0.05). CONCLUSIONS: Ethanol intake preceding H. pylori inoculation could promote the progression of gastric mucosal inflammation in Mongolian gerbils.     

Helicobacter pylori infection promotes gastric carcinogenesis in a mice model

BACKGROUND AND AIM: Debate that Helicobacter pylori might play a causative role in gastric carcinogenesis still exists in spite of the World Health Organization's definition of H. pylori as a class I carcinogen. In order to define the exact role of H. pylori infection in gastric carcinogenesis, we established a mice model of H. pylori infection. METHODS: One hundred and forty-four female C57BL/6 mice were divided into nine groups according to N-methyl-N-nitrosourea (MNU) treatment and H. pylori infection. All mice were killed at the 50th or 80th week after treatment, and their histopathological changes were evaluated according to group. RESULTS: The incidence of gastric adenocarcinoma at the 50th week was 80% in mice treated with both MNU 240 microg/L and H. pylori infection, whereas the incidence was only 27% in mice treated with only MNU 240 microg/L. Although H. pylori caused marked expansion of the proliferative zone at the surface epithelium, H. pylori infection alone caused only chronic atrophic gastritis without any evidence of carcinomas until 80 weeks. The combination of MNU and H. pylori infection also resulted in a significantly higher incidence of gastric adenoma and adenocarcinoma. Significantly higher expressions of proliferating cell nuclear antigen were noted in the gastric mucosa infected with H. pylori compared to controls. CONCLUSIONS: These results clearly demonstrated the role of H. pylori infection, rather than direct carcinogens, in promoting gastric carcinogenesis in a mice model.     

Long-term stress and Helicobacter pylori infection independently induce gastric mucosal lesions in C57BL/6 mice

BACKGROUND: Long-term psychological stresses may have a role in the pathogenesis of peptic ulcer. However, the interaction between stress and Helicobacter pylori infection in the development of peptic ulcer is not established. The aim of this study was to elucidate the roles of long-term stress and H. pylori infection in the development of gastric mucosal lesions in mice. METHODS: The Sydney strain (SS1) of H. pylori was inoculated into the stomach of C57BL/J6 mice. Twelve weeks later, mice with or without H. pylori infection were exposed to long-term repeated water-immersion-restraint stress (WIRS) for 12 h per day, 3 times per week, for 8 weeks. Gastric mucosal lesions were evaluated both macroscopically (ulcer index) and microscopically (Updated Sydney System). RESULTS: The long-term WIRS induced mild inflammation, oedema, interstitial haemorrhage and superficial erosions in the stomach of mice both with and without H. pylori infection. The degree of mucosal inflammation or atrophy in H. pylori-infected mice was not influenced by the stress. In the mice without H. pylori infection, the ulcer index of the stressed mice was greater than that of non-stressed mice (1.66 +/- 0.39 versus 0.17 +/- 0.08, P = 0.007). In the mice with H. pylori infection, the ulcer index (mean +/- s(x)) of the stressed mice was also greater than that of non-stressed mice (2.31 +/- 0.59 versus 0.64 +/- 0.22, P = 0.027). CONCLUSIONS: The present study showed that long-term stress can induce gastric mucosal inflammation and erosions, and this effect may occur independently of H. pylori infection.     

益生菌对感染幽门螺杆菌的C57BL／6小鼠胃黏膜IL-8、IFN—γ以及IL-4、IL-10的调节效应

益生菌对治疗幽门螺杆菌（Hpylori）感染可起有益的作用,但其作用机制尚未完全明确。目的：观察益生菌（乳酸杆菌、双歧杆菌和肠球菌）对感染Hpflori的C57BL／6小鼠胃黏膜IL-8、IFN-γ以及IL-4、IL-10的影响,并初步探讨益生菌治疗Hpylori感染的作用机制。方法：建立H．pylori感染性胃炎动物模型,将32只小鼠随机分为正常对照组、模型组、标准三联治疗组和联合治疗组（益生菌联合标准三联治疗）。治疗4周后处死小鼠,以快速尿素酶试验、Giemsa染色和细菌培养检测Hpylori感染,行HE染色评估胃黏膜组织学变化,ELISA法检测胃黏膜IL-8、IFN-1以及IL-4、IL-10含量。结果：联合治疗组的Hpylori根除率显著高于标准三联治疗组（P〈0．05）。联合治疗组小鼠胃黏膜中性粒细胞浸润程度、慢性炎症评分、IL-8、IFN-γ含量均显著低于模型组和标准三联治疗组（P〈0．05）,但仍显著高于正常对照组（P〈0．05）;与其余三组相比,联合治疗组IL-4和IL-10含量均显著升高（P〈0．05）。结论：益生菌联合以PPI为基础的标准三联疗法可显著提高Hpylori根除率,降低致炎因子IL-8、IFN-γ水平,减轻胃黏膜中性粒细胞的浸润,并促进抗炎因子IL4、IL-10的生成进而诱导Th2细胞免疫应答。