Association of high expression in rat gastric mucosal heat shock protein 70 induced by moxibustion pretreatment with protection against stress injury

AIM:To study the effect of moxibustion on Zusanli or Liangmeng point on gastric mucosa injury in stress-induced ulcer rats and its correlation with the expression of heat shock protein 70 (HSP70). METHODS:Sixty healthy SD rats (30 males,30 females) were divided into control group,injury model group,Zushanli point group,Liangmeng point group. Stress gastric ulcer model was induced by binding cold stress method. Gastric mucosa ulcer injury (UI) index was calculated by Guth method. Gastric mucosa blood flow (GMBF) was recorded with a biological signal analyzer. Protein content and gene expression in gastric mucosal HSP70 were detected by immunohistochemistry (IHC) and reverse transcription polymerase chain reaction (RT-PCR). Thiobarbital method was used to determine malondialdehyde (MDA) content. Gastric mucosal endothelin (ET) and prostaglandin E2 (PGE2) were analyzed by radioimmunoassay. RESULTS:High gastric mucosal UI index,high HSP70 expression,low GMBF and PGF2,elevated MDA and ET were observed in gastric mucosa of rats subjected to cold stress. Moxibustion on Zusanli or Liangmeng point decreased rat gastric mucosal UI index,MDA and ET. Conversely,the expression of HSP70,GMBF,and PGE2 was elevated in gastric mucosa after pretreatment with moxibustion on Zusanli or Liangmeng point. The observed parameters were significantly different between Zusanli and Liangmeng points. CONCLUSION:Pretreatment with moxibustion on Zusanli or Liangmeng point protects gastric mucosa against stress injury. This protection is associated with the higher expression of HSP70 mRNA and protein,leading to release of PGE2 and inhibition of MDA and ET,impairment of gastric mucosal index.

PROTECTIVE EFFECT OF MOXIBUSTION AT SHENQUE(RN 8)ON GASTRIC MUCOSA

Male S.D rats weighing 200g were used(as experimental animals).Moxibus-tion at Shenque(RN 8)was performed for 15 minutes each day.The course lasted for weeks.In ratsundergoing oral infusion of taurocholate,index of gastric mucosal injury were 9.0±6.1 and 4.6±2.5 in two and four week groups respectively.Compared with control group(index:16.8±7.6),Pwas less than 0.05 and 0.01.This indicated that moxibustion had protective effect on gastric mucosalinjury.Time-effect relationship also existed.In experiment of analysis about mechanism of moxibustion,we found that moxibustion.1.stim-ulated the secretion of gastric mucus(P【0.001);2.increased the PGE 2 content in gastric mucosa(P【0.05);3.increased the number of β-endorphin-like immunoactive cells in gastric mucosa(P【0.05);4.enhanced the transformation of lymphocytes(P【0.01);5.reinforced the function of an-tibody-producing cells in the spleen.The results suggested that protective effect of moxibustion might result from the increase in mu-cus,the PGE 2 and the endogenous β-endorphin.It might also be related to the reinforcing effect ofmoxibustion on transformation of lymphocytes and antibody-producing function of spleen cells.

Relationship between trefoil factor 1 expression and gastric mucosa injuries and gastric cancer

AIM:To determine whether trefoil factor 1 (TFF1) is associated with mucosa healing and carcinoma suppression, we assess the expression of trefoil factor 1 in normal and pathologic gastric mucosa. METHODS: TFF1 in normal and pathologic gastric mucosa was assessed by immunohistochemical method, and the average positive A was estimated by Motic Images Advanced 3.0 software. RESULTS: Increased TFF1 was detected in gastritis, gastric ulcer and duodenal ulcer compared with normal mucosa. The same result could be seen in multiple and compound ulcer compared with simple ulcer. There was no significant difference between gastric ulcer and duodenal ulcer, gastritis and simple ulcer respectively. Increased TFF1 was detected in the peripheral mucosa of the gastric adenocarcinoma compared with normal mucosa. The expression of TFF1 in gastric adenocarcinoma was related to the differentiation of adenocarcinoma. The lower the differentiation of adenocarcinoma, the weaker the expression of TFF1. There was no TFF1 expressed in low-differentiated adenocarcinoma. The expression of TFF1 in middle and highly differentiated adenocarcinoma was a little lower than that in normal mucosa. But there was no significant difference. No TFF1 was assessed in esophageal squamous carcinoma and peripheral tissue. There was no significant difference between male and female. CONCLUSION: The expression of TFF1 was higher in gastritis and peptic ulcer than that in normal mucosa, and was also higher in multiple and compound ulcer than in simple ulcer. It seems that TFF1 plays a role in gastric mucosa protection and epithelial restitution. Increased expression of TFF1 in peripheral tissue suggests that TFF1 is associated with mechanism of carcinoma suppression and differentiation. Decreased expression of TFF1 in carcinoma and its relativity to the differentiation suggests that TFF1 is related to gland and cell destruction of carcinoma.

Molecular forms of trefoil factor 1 in normal gastric mucosa and its expression in normal and abnormal gastric tissues

AIM： To study the molecular forms of trefoil factor 1 （TFF1） in normal gastric mucosa and its expression in normal and abnormal gastric tissues （gastric carcinoma, atypical hyperplasia and intestinalized gastric mucosa） and the role of TFF1 in the carcinogenesis and progression of gastric carcinoma and its molecular biological mechanism underlying gastric mucosa protection. METHODS： The molecular forms of TFF1 in normal gastric mucosa were observed by Western blot. The expression of TFF1 in normal and abnormal gastric tissues （gastric carcinoma, atypical hyperplasia and intestinalized gastric mucosa） was also assayed by immunohistochemical method. The average positive AO was estimated by Motic Images Advanced 3.0 software. RESULTS： Three patterns of TFF1 were found in normal gastric mucosa： monomer, dimmer, and TFF1 compound whose molecular weight is about 21 kDa. The concentration of TFF1 compound was the highest among these three patterns. TFF1 was expressed mainly in epithelial cytoplasm of the mucosa in gastric body and antrum, especially around the nuclei. The closer the TFF1 to the lumen, the higher the expression of TFF1, The expression of TFF1 in peripheral tissue of gastric carcinoma （0.51 ± 0.07） was higher than that in normal gastric mucosa （0.44 ± 0.06, P 〈 0.001）. The expression of TFF1 in gastric adenocarcinoma was positively related to the differentiation of adenocarcinoma. The lower the differentiation of adenocarcinoma was, the weaker the expression of TFF1. No TFF1 was expressed in poorlydifferentiated adenocarcinoma. The expression of TFF1 in moderately-well differentiated adenocarcinoma （0.45 ± 0.07） was a little lower than that in normal mucosa （P 〉 0.05）. The expression of TFF1 in gastric mucosa with atypical hyperplasia （0.57 ± 0.03） was significantly higher than that in normal gastric mucosa （P 〈 0.001）. No TFF1 was expressed in intestinalized gastric mucosa. There was no statistically significant difference between the expressions of TFFI in gastric mucosa around the intestinalized tissue （0.45 ± 0.07） and normal gastric mucosa （P 〉 0.05）. CONCLUSION： TFF1 is expressed mainly in epithelial cytoplasm of the mucosa in gastric body and antrum. Its main pattern is TFF1 compound, which may have a greater biological activity than monomer and dimer. The expression of TFF1 in peripheral mucosa of gastric ulcer is higher than that in mucosa 5 cm beyond the ulcer, indicating that TFF1 plays an important part in protection and restitution of gastric mucosa. The expression of TFF1 is increased in peripheral tissues of gastric carcinoma and gastric mucosa with atypical hyperplasia, but is decreased in cancer tissues, implying that TFF1 may be related to suppression and differentiation of carcinoma. The weaker expression of TFF1 in poorly-differentiated carcinoma may be related to the destruction of glands and cells in cancer tissues and the decrease in secretion of TFF1.

芍药甘草汤对大鼠酒精性胃溃疡的保护作用及其可能机制研究

目的:本研究旨在评估芍药甘草汤(SGD)对大鼠酒精性胃溃疡(GU)的保护作用及其可能机制,以期为临床治疗提供参考。方法:采用单次灌胃10 mL/kg 75%乙醇建立大鼠胃溃疡模型,对胃组织进行组织病理学检查。用双抗体夹心法测定胃组织中肿瘤坏死因子-α(TNF-α)、表皮生长因子(EGF)、前列腺素E2(PGE2)、超氧化物歧化酶(SOD)和血浆硫代巴比妥酸反应物质(TBARS)水平。应用网络药理学研究方法,进一步研究SGD治疗GU的可能机制。结果:组织学特征显示,酒精性GU大鼠的胃组织在整个胃黏膜层均有明显的损伤,而SGD治疗组大鼠的胃黏膜损伤明显减轻。标志物检测显示,SGD(9.90 g/kg)组和SGD(19.80 g/kg)组TNF-α的水平显著下降(分别为模型组的87.17%和86.50%,P<0.01)。SGD(9.90 g/kg)组和SGD (19.80 g/kg)组PGE2水平均显著高于模型组(分别为模型组的172.40%和220.86%,P<0.01)。与模型组比较,SGD(19.80 g/kg)组SOD水平均显著升高(为模型组的162.13%,P<0.01)。而在脂质过氧化方面,SGD(9.90 g/kg)组、SGD(19.80 g/kg)组TBARS水平显著下降(分别为模型组的78.66%、71.83%,P<0.01)。结论:SGD对乙醇所致GU有改善作用。此外,本研究还揭示了SGD治疗GU的多组分、多靶点、多途径的特点,为进一步的药物开发研究提供了基础。

200∶1库拉索芦荟凝胶冻干粉对大鼠胃黏膜的保护作用研究

本文以50只SPF级SD大鼠为试验对象,设置0.167 g/kg BW低剂量组、0.333 g/kg BW中剂量组、1.000 g/kg BW高剂量组、空白对照组(CK1)、模型对照组(CK2)5个处理,每个处理10只大鼠,其中:低、中、高剂量组分别灌胃200∶1库拉索芦荟凝胶冻干粉,空白对照组(CK1)和模型对照组(CK2)分别灌胃相同体积的蒸馏水。各处理灌胃体积均为10 mL/kg BW,每天1次,连续灌胃30 d。之后,除空白对照组(CK1)外,其他处理以无水乙醇作为急性胃黏膜损伤剂给予大鼠。对大鼠进行解剖,比较各处理大鼠胃黏膜损伤积分指数、胃黏膜病理组织学检查病变总积分,研究200∶1库拉索芦荟凝胶冻干粉对无水乙醇引起的大鼠急性胃黏膜损伤能否产生治疗效果。结果表明:200∶1库拉索芦荟凝胶冻干粉0.167 g/kg BW低剂量组、0.333 g/kg BW中剂量组、1.000 g/kg BW高剂量组对大鼠体质量无明显影响;200∶1库拉索芦荟凝胶冻干粉0.333 g/kg BW中剂量组大鼠胃黏膜损伤积分指数、胃黏膜病理组织学检查病变总积分显著低于模型对照组(CK2)(P<0.05)。可见,200∶1库拉索芦荟凝胶冻干粉对于大鼠胃黏膜有着辅助保护功能。

鳕鱼皮胶原肽对大鼠胃黏膜损伤的保护作用及其机制

目的:探究不同分子质量段的鳕鱼皮胶原肽对酒精性胃黏膜损伤的保护效果及相关机理。方法:从鳕鱼皮中提取胶原蛋白并用复合酶酶解,制备不同分子质量段的胶原肽,采用高体积分数酒精诱导的大鼠急性胃黏膜损伤模型,观察统计胃黏膜损伤程度并对胃部组织及血清的生理生化指标进行检测。结果;与模型组相比,胶原肽能够减轻大鼠胃腺的出血损伤,降低胃组织中Ca^(2+)含量及髓过氧化物酶活力(P<0.05);其中,中分子质量胶原肽效果最好,该组大鼠胃黏膜损伤指数降至9.21%(P<0.01),损伤抑制率为57.16%;胶原肽能提高胃组织中糖蛋白含量(P<0.05),降低胃组织中丙二醛含量,提高胃组织超氧化物歧化酶活力及血清中谷胱甘肽的含量(P<0,05)。结论:胶原肽能够通过增强大鼠胃黏膜屏障及机体抗自由基氧化水平,产生对急性胃黏膜损伤的保护作用。

三叶因子1表达与胃粘膜损伤及胃癌的关系

目的测定三叶因子1在正常及病理条件下胃粘膜中的表达情况,探讨TFF1在胃粘膜损伤修复及胃癌抑制中的作用及意义。方法应用免疫组化方法测定正常及不同病理条件下胃粘膜中TFF1的表达情况,通过图像分析软件分析其阳性信号平均光密度值了解其表达情况。结果胃炎、胃溃疡及十二指肠球部溃疡患者TFF1表达明显高于正常胃粘膜;多发/复合性溃疡患者TFF1表达高于单发的消化性溃疡患者;胃溃疡患者与十二指肠球部溃疡患者、胃炎患者与单一消化性溃疡患者表达相比均无统计学差异;胃腺癌患者癌旁组织表达明显高于正常胃粘膜,而腺癌组织的表达强度则与癌组织的分化程度呈正比,分化程度愈低,表达愈弱,低分化腺癌无阳性表达,中、高分化腺癌表达略低于正常粘膜,但二者对比无统计学差异;食管鳞癌及癌旁组织均无阳性表达;各组男女对比均无统计学差异。结论TFF1在胃炎及消化性溃疡中表达升高,且在多发/复合性溃疡中的表达较单发溃疡表达升高,即粘膜损伤越严重其表达越强,提示其在胃粘膜保护及促进上皮重建机制中具有一定的作用。TFF1在癌旁组织中表达增强提示其可能与肿瘤抑制及分化机制有关,而在癌组织中表达减弱,且分化程度越低表达越弱可能与癌组织腺体及细胞破坏、TFF1的分泌减少有关。

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。

乙醇性胃粘膜损伤及其保护作用的研究进展

本文主要对乙醇的特点及其在胃肠道中的代谢,乙醇对胃粘膜的损伤作用,对胃粘膜防御因子和自由基的影响,胃粘膜保护机制,以及保护胃粘膜的药物和生物活性物质的研究进展作简要介绍。

三叶因子在正常胃黏膜中存在的分子形式及其与癌变的关系

目的研究三叶因子1(TFF1)在正常胃黏膜中存在的分子形式及其在正常、胃癌、不典型增生及肠化胃黏膜中的表达,探讨TFF1在胃癌的发生、发展中的作用及其胃黏膜保护作用的分子生物学机制。方法采用Westernblotting方法观察TFF1在正常胃黏膜中存在的分子形式,并采用免疫组化方法测定正常、胃癌、不典型增生及肠化胃黏膜中TFF1的表达情况,通过图像分析软件分析其阳性信号平均光密度值了解其表达情况。结果TFF1在人正常胃黏膜中以3种形式存在,即单聚体、二聚体和Mr21000的TFF1与某种分子结合而成的复合物,其中TFF1复合物的含量最高。TFF1主要在人胃体及胃窦黏膜上皮表面细胞胞质中表达,核周聚集较明显,越靠近腔面的细胞表达越强。胃腺癌患者癌旁组织TFF1表达(0.51±0.07)明显高于正常胃黏膜(0.44±0.06,P<0.001),而腺癌组织的表达强度则与癌组织的分化程度呈正比,分化程度愈低,表达愈弱,低分化腺癌无阳性表达,中、高分化腺癌表达(0.41±0.07)略低于正常黏膜(P>0.05)。不典型增生胃黏膜TFF1表达(0.57±0.03)明显高于正常胃黏膜(P<0.001);肠化胃黏膜无TFF1阳性表达,但肠上皮化生周围的胃黏膜TFF1表达(0.45±0.07)与正常胃黏膜相比无统计学差异(P>0.05)。结论TFF1在胃黏膜保护及修护方面具有重要的作用,其在胃黏膜中主要以复合物的形式存在。TFF1可能与肿瘤抑制及分化机制有关。

丹参粉针对大鼠应激性溃疡胃黏膜保护作用的实验研究

目的探讨丹参粉针对大鼠应激性溃疡胃黏膜保护作用及机制。方法实验选用健康的SD雄性大鼠32只,分为空白对照组、浸水束缚应激方法复制应激性溃疡模型对照组、丹参粉针预防组用80mg·kg^(-1)体重(3m L)灌胃2次后造模。造模后察胃黏膜大体标本,计算损伤指数,并行病理切片,比色法检测各组大鼠血清超氧化物歧化酶(SOD)、胃黏膜还原型谷胱甘肽(GSH)含量、酶联免疫吸附竞争法检测胃黏膜前列腺素E2(PGE2)的含量。结果模型组与空白对照组比较损伤指数增加(P<0.05),丹参预防组与模型对照组比较损伤指数降低(P<0.05),丹参预防组与空白对照组比较差异无统计学意义(P>0.05);丹参预防组比模型对照组SOD、PGE_2、GSH活性增高(P<0.05或<0.01),与空白组比较差异均无统计学意义(P均>0.05);模型组与空白对照组比较SOD、PGE_2、GSH活性降低(P<0.05或<0.01)。结论丹参粉针对应激损伤的胃黏膜有良好的保护作用。

丹参三七药对对大鼠酒精损伤后胃及肝脏的保护作用

目的研究丹参三七药对对大鼠酒精损伤后胃黏膜及肝脏的保护作用。方法取SD大鼠80只,按体质量随机分为4组,每组20只,空白对照组,模型对照组,高、低2个剂量组(2.4和0.8 g/kg),灌胃给药,每日1次,连续30 d。实验末乙醇灌胃造成大鼠急性酒精损伤模型,游标卡尺测量胃黏膜的损伤面积,试剂盒测定肝组织中丙二醛(MDA)、三酰甘油(TG)、还原型谷胱甘肽(GSH)含量及胃组织中蛋白酶原(PG)、生长抑素(SS)的含量,对胃部及肝脏进行病理检查。结果高剂量大鼠肝脏组织中的MDA及TG含量降低、GSH含量升高,胃黏膜组织中的PG、SS含量升高,与模型对照组相比,差异均有统计学意义。胃及肝组织的病理结果表明,高剂量组大鼠的胃黏膜病变总积分及肝脏病理总分均明显小于模型对照组,且差异有统计学意义。结论丹参三七药对对酒精性肝损伤及胃黏膜损作有一定的保护作用。

艾灸对脊髓横断术后大鼠胃黏膜组织相关因子及热休克蛋白70表达的影响

目的观察艾灸对大鼠胃黏膜组织白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、表皮生长因子(EGF)及热休克蛋白70(HSP70)表达的影响,探讨艾灸对胃黏膜的保护效应与脊髓的关系。方法实验大鼠采用无水乙醇+阿司匹林灌胃制作胃黏膜损伤模型。将48只SD大鼠随机分为正常组、模型组、艾灸模型组和艾灸+脊髓横断组,每组12只。艾灸+脊髓横断组大鼠行脊髓横断手术,并予以艾灸干预。GUTH法计算胃黏膜组织损伤指数(UI),ELISA检测血清IL-1β、TNF-α和EGF含量;Western blot检测胃黏膜组织HSP70蛋白表达。结果与模型组比较,艾灸模型组大鼠胃黏膜组织UI下降、EGF含量升高,血清IL-1β、TNF-α含量降低(P<0.05,P<0.01);与艾灸模型组比较,艾灸+脊髓横断组大鼠胃黏膜组织UI升高、EGF含量降低,血清IL-1β、TNF-α含量升高(P<0.05,P<0.01);与模型组比较,艾灸模型组和艾灸+脊髓横断组大鼠胃黏膜组织HSP70蛋白表达均明显增加(P<0.01)。结论脊髓是艾灸对胃黏膜损伤修复与保护因子表达的重要调节途径。

泮托拉唑和吉法酯治疗双联抗血小板所致上消化道出血的对比研究

目的探讨质子泵抑制剂(proton pump inhibitor,PPI)泮托拉唑和胃黏膜保护剂吉法酯对经皮冠状动脉介入(percutaneous coronary intervention,PCI)术后服用双联抗血小板药物患者上消化道出血的预防效果。方法 1263例PCI术后服用肠溶阿司匹林合并氯吡格雷纳入本研究,按治疗小组分为4组:常规治疗组(n=332)、PPI组(n=318)、胃黏膜保护剂组(n=299)、PPI+胃黏膜保护剂组(n=314)。随访6个月,观察患者的消化道症状、上消化道出血、主要心脏不良事件(major adverse cardiac events,MACE)、不良反应等。结果 52例6个月内发生上消化道出血,其中常规治疗组21例,PPI组9例,胃黏膜保护剂组15例,PPI+胃黏膜保护剂组7例,4组6个月内上消化道出血发生率有统计学差异(χ~2=8.883,P=0.031),其中常规治疗组显著高于PPI组和PPI+胃黏膜保护剂组(P<0.05),其他各组间消化道出血发生率无统计学差异(P>0.05)。术后3个月内发生上消化道出血34例,占全部上消化道出血65.4%(34/52),4组消化道出血的发生时间无统计学差异(χ2=4.212,P=0.648)。结论泮托拉唑或泮托拉唑联合吉法酯口服可降低PCI术后双联抗血小板药物患者上消化道出血的发生率。上消化道出血的预防性治疗应从PCI术后第1天开始,至少维持3~6个月,甚至更长。

中药对胃黏膜保护作用的实验研究进展

消化性溃疡、急性胃黏膜病变是临床常见病、多发病 ,中药防治胃黏膜损伤有其自身特点及优势。近年来许多学者在此领域作了大量研究工作 ,发现并证实许多中药单味药及复方制剂具有明显的胃黏膜保护作用 ,阐明了中药可通过如下多种途径及机制达到防治胃黏膜损伤的作用 :抗胃酸、胃蛋白酶 ;强化胃黏膜、黏液屏障 ;改善调节胃黏膜血流 ;诱导胃黏膜内源性保护因子的合成和释放 ,增强胃黏膜细胞保护作用 ;抗自由基损伤等。

银杏叶提取物的胃粘膜保护作用

采用大鼠束缚－冷冻应激模型和小鼠无水乙醇损伤模型观察银杏叶提取物（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。结果表明，ＧｂＥ（２５，５０，１００ｍｇ／ｋｇ，ｂｉｄ×５ｄ，ｉｇ）可剂量依赖性地抑制束缚－冷冻应激（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５８．１１％，４２．９９％和３１．２３％；用药组乙醇诱发的胃粘膜损伤指数降至对照组的６１．５４％，３６．０６％和２５．６４％；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１ｈ，胃粘膜和血清中的ＭＤＡ含量显著升高（Ｐ＜０．０１），而ＧｂＥ（２５，５０，１００ｍｇ／ｋｇｉｇ）预处理则可以明显抑制ＭＤＡ的升高。因此认为ＧｂＥ具有胃粘膜保护作用，并且与西米替丁在治疗胃溃疡方面具有协同作用，这些作用可能与其抗氧化作用相关。

雷贝拉唑和替普瑞酮治疗双联抗血小板所致上消化道出血的对比研究

目的探讨质子泵抑制剂(PPI)雷贝拉唑和胃黏膜保护剂替普瑞酮对经皮冠状动脉介入(PCI)术后服用双联抗血小板药物患者上消化道出血的预防效果。方法400例PCI术后服用肠溶阿司匹林合并氯吡格雷纳入本研究,按治疗小组分为4组:常规治疗组100例、PPI组100例、胃黏膜保护剂组100例、PPI+胃黏膜保护剂组100例。随访6个月,观察患者的上消化道出血发生率及严重程度、主要心脏不良事件(MACE)、不良反应等。结果4组中6个月内发生上消化道出血28例,其中常规治疗组15例(大出血2例,小出血4例,轻微出血9例),PPI组3例(轻微出血),胃黏膜保护剂组9例(小出血3例,轻微出血6例),PPI+胃黏膜保护剂组1例(轻微出血),4组6个月内上消化道出血发生率差异有统计学意义(χ2=18.43,P<0.01),其中常规治疗组明显高于PPI组和PPI+胃黏膜保护剂组(P<0.05),其他各组间消化道出血发生率差异无统计学意义(P>0.05)。术后3个月内发生上消化道出血27例,占全部上消化道出血96%。4组MACE发生差异无统计学意义(χ2=4.05,P=0.262)。结论雷贝拉唑或雷贝拉唑联合替普瑞酮口服可降低PCI术后双联抗血小板药物患者上消化道出血的发生率。上消化道出血的预防性治疗应从PCI术后第1天开始,至少维持3~6个月,甚至更长。

三油酸甘油酯抗胃粘膜损伤及作用机制

考察了三油酸甘油酯对无水乙醇所致大鼠胃粘膜损伤的保护作用及其对抗aspirin、reser pine所致小鼠胃溃疡的作用 .并进一步探讨了三油酸甘油酯抗溃疡作用的机制 .实验结果表明 ,三油酸甘油酯可降低上述各模型中大鼠及小鼠的溃疡指数 ,其作用是以增强胃的防御因子为主 .主要机制研究表明 ,三油酸甘油酯是通过促进胃内前列腺素E2 (PGE2 )

胶体枸橼酸铋钾预防阿司匹林所致大鼠胃粘膜损伤的研究

目的 :研究枸橼酸铋钾对阿司匹林所致大鼠胃粘膜损伤的预防保护作用及其机制。方法 :采用阿司匹林腹腔注射造成Wistar大鼠急性胃粘膜损伤模型。实验动物分为空白对照组、单纯损伤组、枸橼酸铋钾保护组和米索前列醇保护组。保护组分别用枸橼酸铋钾和米索前列醇灌胃 ,其后用阿司匹林行腹腔注射 ,然后分别测定各组的胃粘膜溃疡指数、胃粘膜血流、胃粘膜氨基己糖含量等指标 ,并观察大体及显微镜下组织学变化 ,以评价胃粘膜损伤程度及药物的预防保护效果。结果 :枸橼酸铋钾保护组与单纯损伤组比较 ,胃粘膜损伤指数明显下降(P <0 .0 1 ) ,胃粘膜血流增加 (P <0 .0 1 ) ,胃粘膜氨基己糖含量增加 (P <0 .0 1 )。且与米索前列醇保护组相比胃粘膜溃疡指数、粘膜血流、氨基己糖含量无明显差异。结论 :枸橼酸铋钾对阿司匹林所致的大鼠急性胃粘膜损伤有明显预防保护作用 ,其保护作用与米索前列醇相当 ;作用机制与增加胃粘膜血流 。