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食管下段黏膜上皮细胞间隙影响因素的实验研究
中文摘要

 目的: 近年来有不少研究提出食管下段黏膜鳞状上皮细胞间隙增宽(dilated intercellular spaces, DIS)是胃食管反流病(gastroesophageal reflux disease, GERD)患者早期、特异的超微结构改变,无论食管是否存在内镜下可见的黏膜破损;抑酸治疗可以使DIS恢复正常。因此,许多学者认为DIS可以作为内镜下未见食管黏膜破损的非糜烂性反流病(non-erosive reflux disease, NERD)非常重要的指征,灵敏度及特异度均较高,有望成为NERD诊断和治疗中重要的临床指标。但酸反流是否是造成DIS的唯一因素?有报道认为存在食管不适症状的病人(不论是否有酸反流)亦存在DIS。其他常见损伤因素,如乙醇、非甾体类抗炎药(NSAIDs)、皮质类固醇、应激等,在导致胃黏膜损伤的同时,是否也引起食管下段黏膜上皮细胞间隙的改变,尚不明确。临床常用的黏膜保护剂能否通过减小损伤因素引起的上皮细胞间隙增宽来增强黏膜防御修复机制,从而减轻黏膜损伤,目前尚无研究。本研究旨在观察大鼠实验性食管、胃黏膜损伤与保护的超微结构改变,并探讨细胞黏附分子CD15表达水平与食管下段黏膜上皮细胞间隙增宽的关系,为NERD发病机理、临床诊断与鉴别、损伤及保护因素的作用提供实验依据。 方法: 1.多种损伤因素对大鼠食管下段黏膜上皮细胞间隙的影响:SPF级、雄性SD 大鼠随机分为8组,实验组每组6只,对照组每组5只。处理如下:(1)正常对照组:实验当天不施加任何处理因素,7小时后乙醚麻醉。(2)生理盐水灌胃组:实验当天生理盐水1ml灌胃,1小时后麻醉。(3)生理盐水皮下注射组:每日颈部皮下注射生理盐水2ml 一次,连续4日,第4日注射生理盐水后8小时麻醉。(4)水浸束缚应激组:实验当天将束缚的大鼠保持正立位置于20±1℃的恒温水浴中,水面达胸骨剑突水平,7小时后麻醉。(5)盐酸灌胃组:实验当天0.7mol/L盐酸1ml灌胃,1小时后麻醉。(6)乙醇灌胃组:实验当天无水乙醇1ml灌胃,1小时后麻醉。(7)阿司匹林灌胃组:实验当天阿司匹林溶液约1ml (300㎎/㎏,溶于2%碳酸氢钠溶液中)灌胃,1小时后麻醉。 (8)波尼松龙皮下注射组:每日颈部皮下注射醋酸波尼松龙约2ml (250㎎/㎏/d) 一次,连续4日,第4日注射波尼松龙8小时后麻醉。所有大鼠按上述方法处理,麻醉前禁食24小时,麻醉状态下取大鼠食管和胃大体观察,并于齿状线上方0.5~1㎝处取食管黏膜组织,分别进行常规病理组织学检查(苏木素-伊红染色)和透射电子显微镜检测,计算上皮细胞间隙宽度(μm);剩余食管黏膜组织迅速放入液氮中速冻,然后放-80℃冰箱保存。 2.埃索美拉唑抑酸预处理对水浸束缚应激和阿司匹林诱发的大鼠食管下段黏膜上皮细胞间隙增宽的影响:(1)水浸束缚应激模型:SD大鼠随机分为埃索美拉唑组和生理盐水对照组,每组6只,分别给予埃索美拉唑(5㎎/㎏/d)和等量生理盐水5日。第5日给药或生理盐水后2小时,再给以水浸束缚应激。麻醉状态下取大鼠食管下段黏膜组织,电镜检测上皮细胞间隙宽度(Mm)的变化。(2)阿司匹林模型:第5日给埃索美拉唑或生理盐水后2小时,阿司匹林约1ml (300㎎/㎏,溶于2%碳酸氢钠溶液中)灌胃,1小时后麻醉,余实验方法同水浸束缚应激模型。 3.铝碳酸镁等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: (1)乙醇模型:SD大鼠随机分为7组,每组12只。分别给予铝碳酸镁、麦滋林-S、替普瑞酮、吉法酯、硫糖铝、瑞巴派特或等量生理盐水4日。第4日给药或生理盐水一次,2小时后,再经口给无水乙醇1ml造模。1小时后处死动物,取大鼠胃大体标本,计算各组大鼠胃黏膜损伤长度(㎜)作为损伤指数,并取对照组和铝碳酸镁组大鼠胃大弯距储存胃和黏膜胃交界线0.5㎝处未损伤胃黏膜组织,电镜检测上皮细胞间隙宽度(μm)的变化。 (2)盐酸模型:经口给0.7mol/L盐酸1ml造模,余实验方法同乙醇模型。(3)阿司匹林淡盐酸模型:经口给阿司匹林约1ml (300㎎/㎏,用2%碳酸氢钠溶液配),1小时后再灌给0.1 mol/L盐酸约1ml (5ml/㎏)造模,余实验方法同乙醇模型。(4)波尼松龙模型:动物分组及给药剂量和种类同其他模型,给药或生理盐水5日,第2~5日每日颈部皮下注射醋酸波尼松龙约2ml (250㎎/㎏/d) 一次,第5日注射波尼松龙8小时后处死动物,取大鼠胃大体标本,用Guth方法计算胃黏膜损伤指数(分),并取对照组和铝碳酸镁组大鼠胃黏膜组织,电镜检测上皮细胞间隙宽度(μm)的改变。 4.预防性应用铝碳酸镁对水浸束缚应激和阿司匹林模型大鼠食管下段黏膜及胃黏膜超微结构改变的作用:(1)水浸束缚应激模型:SD大鼠随机分为2组,每组6只。分别预防性给予铝碳酸镁(375㎎/㎏/d)和等量生理盐水4日。第4日给药或生理盐水一次,2小时后,再给以水浸束缚应激。麻醉状态下取大鼠胃大体标本,用Guth方法计算胃黏膜损伤指数(分),并取大鼠食管下段和胃黏膜组织,电镜检测上皮细胞间隙的宽度(μm)。(2)阿司匹林模型:第4日给铝碳酸镁或生理盐水一次,2小时后,阿司匹林约1ml (300㎎/㎏,溶于2%碳酸氢钠溶液中)灌胃,1小时后麻醉,余实验方法同水浸束缚应激模型。 5.细胞黏附分子CD15表达水平变化与食管下段黏膜上皮细胞间隙增宽的关系:应用蛋白质免疫印迹(Western blot)方法检测第一部分实验中正常对照组、生理盐水灌胃组、水浸束缚应激组和阿司匹林灌胃组大鼠食管黏膜组织中CD15表达水平的变化。 结果: 1.多种损伤因素对大鼠食管下段黏膜上皮细胞间隙的影响:大鼠胃黏膜均有不同程度、多发、点状或条索状的淤血、糜烂、溃疡或出血病灶;食管黏膜大体观察及常规病理组织学检查均正常,无糜烂、出血、溃疡及炎症等改变。正常对照组、生理盐水灌胃组、生理盐水皮下注射组、水浸束缚应激组、盐酸灌胃组、乙醇灌胃组、阿司匹林灌胃组及波尼松龙皮下注射组大鼠食管下段黏膜平均上皮细胞间隙分别为0.13±0.02 μm、0.19±0.05 μm、0.14±0.03 μm、0.38±0.05 μm、0.24±0.03 μm、0.25±0.10 μm、0.32±0.12 μm 和0.20±0.03μm。组间比较显示,水浸束缚应激组细胞间隙显著大于正常对照组(P<0.01),阿司匹林灌胃组细胞间隙显著大于生理盐水灌胃组(P<0.01 );盐酸灌胃组与生理盐水灌胃组相比、乙醇灌胃组与生理盐水灌胃组比较、波尼松龙皮下注射组与生理盐水皮下注射组相比,细胞间隙差异均无统计学意义(P>0.05)。 2.埃索美拉唑抑酸预处理对水浸束缚应激和阿司匹林诱发的大鼠食管下段黏膜上皮细胞间隙增宽影响不大:两种模型中,埃索美拉唑组大鼠食管下段黏膜上皮细胞间隙与生理盐水对照组比较差异均无统计学意义(水浸束缚应激模型:0.35±0.05 μm vs. 0.37±0.05 μm;阿司匹林模型:0.24±0.02 μm vs. 0.27±0.03 μm), P>0.05。 3.铝碳酸镁等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:乙醇、盐酸、阿司匹林淡盐酸、波尼松龙诱发的四种胃黏膜损伤模型中,各黏膜保护剂组大鼠胃黏膜损伤指数均显著小于生理盐水对照组(P<0.05),其中铝碳酸镁组与对照组的差异性更显著(P<0.01)。同时铝碳酸镁组大鼠胃黏膜上皮细胞间隙显著小于生理盐水对照组(P<0.05)。 4.预防性应用铝碳酸镁对水浸束缚应激和阿司匹林诱发的大鼠食管下段黏膜上皮细胞间隙增宽影响不大,两种模型中,铝碳酸镁组大鼠食管下段黏膜上皮细胞间隙与生理盐水对照组比较,差异均无统计学意义(水浸束缚应激模型: 0.34±0.04 μm vs. 0.37±0.05 μm;阿司匹林模型:0.23±0.01 μm vs. 0.25±0.02 μm), P>0.05。预防性应用铝碳酸镁后,阿司匹林模型中铝碳酸镁组大鼠胃黏膜损伤指数(分)及上皮细胞间隙均显著小于生理盐水对照组(损伤指数:4.0±1.4 vs. 12.7±5.5;细胞间隙:0.21 ±0.01 μm vs. 0.28±0.01 μm), P<0.05;水浸束缚应激模型中铝碳酸镁组大鼠胃黏膜损伤指数(分)及上皮细胞间隙与生理盐水对照组比较均无统计学差异(损伤指数:9.0±4.1 vs. 15.8±7.4;细胞间隙:0.34±0.03 μm vs. 0.37±0.06 μm), P>0.05。 5.细胞黏附分子CD15表达水平变化与食管下段黏膜上皮细胞间隙增宽的关系:不同组大鼠食管黏膜组织中CD15蛋白的条带密度不同,带宽不同,着色浓度也不同,反映了 CD15蛋白表达水平的不同,即正常对照组和生理盐水灌胃组大鼠CD15表达水平较高,水浸束缚应激组和阿司匹林灌胃组大鼠CD15蛋白表达水平则明显下降。半定量分析显示,食管黏膜组织中CD15蛋白条带的相对光密度值如下:正常对照组大鼠0.32±0.06,水浸束缚应激组大鼠为0.17±0.07,差异有统计学意义(P<0.01);阿司匹林灌胃组大鼠0.17±0.07,显著低于生理盐水灌胃组大鼠的0.29±0.06 (P<0.01)。 结论: 1.水浸束缚应激和阿司匹林在诱发大鼠胃黏膜损伤的同时,可以引起食管下段黏膜上皮细胞间隙增宽,并且出现于食管大体和常规病理组织学改变之前;上皮细胞间隙增宽是食管黏膜上皮屏障功能损伤的一个早期、敏感的超微结构改变。我们实验中所用浓度、剂量和作用时间的盐酸、乙醇及波尼松龙可导致大鼠胃黏膜损伤,但对大鼠食管下段黏膜上皮细胞间隙没有影响。 2.埃索美拉唑抑酸预处理对水浸束缚应激和阿司匹林诱发的大鼠食管下段黏膜上皮细胞间隙增宽没有影响,水浸束缚应激及阿司匹林引起的大鼠食管下段黏膜上皮细胞间隙增宽可能与酸关系不大。 3.铝碳酸镁、麦滋林-S、替普瑞酮、吉法酯、硫糖铝、瑞巴派特等六种常用黏膜保护剂对乙醇、盐酸、阿司匹林淡盐酸和泼尼松龙诱发的大鼠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。铝碳酸镁可以显著减小损伤因素引起的大鼠胃黏膜上皮细胞间隙增宽,从细胞学水平进一步证实了铝碳酸镁的黏膜保护作用机制。 4.预防性应用铝碳酸镁对水浸束缚应激和阿司匹林诱发的大鼠食管下段黏膜上皮细胞间隙增宽没有影响。预防性应用铝碳酸镁对阿司匹林诱发的大鼠胃黏膜损伤有保护作用,并能显著减小大鼠胃黏膜上皮细胞间隙增宽;但对水浸束缚应激诱发的大鼠胃黏膜损伤保护作用不明显,大鼠胃黏膜上皮细胞间隙也无改变。 5.水浸束缚应激和阿司匹林模型大鼠食管黏膜组织中CD15蛋白表达水平分别较正常对照和生理盐水灌胃大鼠显著下降;细胞粘附分子CD15表达水平下调可能与大鼠食管下段黏膜上皮细胞间隙增宽有关。 [关键词]食管;胃;黏膜损伤与保护;上皮细胞间隙;细胞粘附分子;CD15

英文摘要

 Objectives: Recently, it has been reported in several studies that dilated intercellular spaces (DIS) within the lower esophageal mucosal epithelium was an extremely sensitive and specific marker of the damage in gastroesophageal reflux disease (GERD), whether there were mucosal damages or not under endoscopy. Treatment of patients with PPI (proton pump inhibitor) made DIS to normal width. Many researchers regarded DIS as an important marker of non-erosive reflux disease (NERD), which has no mucosal damages within the esophageal mucosa under endoscopy. Is refluxed acid the only factor that leads to DIS? It had been suggested in some reports that patients with esophageal discomfort had DIS, no matter there was acid reflux or not. Do the other damaging factors which always lead to gastric lesions induce DIS within the lower esophageal mucosal epithelium? Do the mucosal protective drugs used frequently in clinics have effects on DIS? The objectives of this study were to (a)observe the ultrastructrual changes in the esophageal and gastric mucosal lesions and protection in rats, (b)investigate relationship between the expression level of cell adhesion molecule CD15 and DIS in the lower esophageal mucosal epithelium, and (c)provide useful experimental data on the study of NERD. Materials and Methods: Part Ⅰ: Influences of different damaging factors on the intercellular space within lower esophageal mucosal epithelium in rats. Male Sprague-Dawley (SD) strain SPF rats were divided into 8 groups randomly (5 or 6 rats per group) and were treated as follows: (1) Group of normal controls: the rats remained untreated in their home cage for 7 hr, and then they were anesthetized using diethyl ether. (2) Group of rats with normal saline (N.S.) intragastric administration: 1ml, once, and one hour after administration the rats were anesthetized. (3) Group of rats with N.S. hypodermic injection: 2ml/d, qd, 4 days. The rats were anesthetized 8 hours after the last injection. (4) Group of rats with water immersion and restraint stress (WIRS): the four limbs of each rat were bouned on a board, and then the rats were immersed in water in a head-up vertical position up to the level of the xiphoid process at a temperature of 20±1 degree for 7 hr. Then they were anesthetized. (5) Group of rats with 0.7mol/L hydrochloric acid intragastric administration: 1 ml, once, and one hour after administration the rats were anesthetized. (6) Group of rats with absolute ethanol intragastric administration: 1ml, once, and the rats were anesthetized one hour after administration. (7) Group of rats with aspirin intragastric administration: 300㎎/㎏, dissolved in 1ml of 2% sodium bicarbonate (NaHCO₃) solution, once, and the rats were anesthetized one hour after administration. (8) Group of rats with prednisolone hypodermic injection: 250㎎/㎏/d, in a volume of 2ml, qd, 4 days. The rats were anesthetized 8 hours after the last injection. All rats were treated as above, and they were fasting for 24 hours before anaesthesia. Esophageal mucosal biopsies from 0.5-1 ㎝ above Z-line were taken to measure the intercellular space width (μm) within the epithelium by transmission electron microscopy (TEM) and to access histological changes by hematoxylin and eosin (H-E) staining. The remained esophageal mucosal biopsies were put into the liquid nitrogen immediately, and then were stored in the refrigerator of -80 degree. Part Ⅱ: Influences of pretreatment with esomeprazole on DIS within the lower esophageal mucosal epithelium of rats induced by WIRS and aspirin. (1) Model of rats with WIRS: SD rats were divided into 2 groups randomly (6 rats per group) and were treated with esomeprazole (5㎎/㎏/d) or N.S. intragastric administration, in a volume of 2ml seperately, qd, for 5 days. On the 5〓 day, 2 hours after administration all the rats underwent WIRS. After anaesthesia, the biopsies of the lower esophageal mucosa were taken to analyze the intercellular spaces width (μm) by TEM. (2) Model of rats with aspirin intragastric administration: After 5 days of esomeprazole or N.S. intragastric administration, all the rats were treated with aspirin (300㎎/㎏, dissolved in 1ml of 2% NaHCO₃ solution) intragastric administration, once. One hour later, the rats were anesthetized, and the rest procedures were similar to those applied in the model of rats with WIRS. Part Ⅲ: Protective effects of Hydrotalcite and other mucosal protective agents against experimental gastric mucosal lesions and the changes in the gastric mucosal ultrastructure in rats. (1) In the model of ethanol induced lesion, a total of 84 male SD rats were divided into 7 groups randomly (12 rats per group). Each group received oral dose of Hydrotalcite, Marzulene-S, Teprenone, Gefarnate, Sucralfate, Rebamipide or N.S. for 4 days respectively. On the 4〓 day, 2 hours after one of the agents were given the rats were administrated 1ml of absolute ethanol orally. One hour later, the rats were sacrificed and the gastric lesion length (㎜) was measured as Ulcer Index (UI). The gastric mucosal tissues of the control group and the Hydrotalcite group were obtained to measure the intercellular space width (μm) under TEM. (2) In the model of hydrochloric acid induced lesion, 1ml of 0.7mol/L hydrochloric acid was administrated orally. All of the rest procedures were the same as those applied in the ethanol model. (3) In the model of aspirin induced lesion, aspirin (300㎎/㎏, dissolved in 1ml of 2% NaHCO₃ solution) and 0.1mol/L hydrochloric acid (5ml/㎏) were administrated orally. All of the rest procedures were the same as those applied in ethanol model in the 84 rats. (4) In the model of prednisolone induced lesion, each group was administrated orally by the 6 mucosal protective agents or N.S. for 5 days. During the 2〓-5〓 days, prednisolone (250㎎/㎏/d) were daily injected subcutaneously. Rats were sacrificed on the 5〓 day. The UI was measured by Guth's method (scores), and the gastric mucosal tissues of the control group and the Hydrotalcite group were obtained to measure the intercellular space width (μm) under TEM. Part Ⅳ: Effects of Hydrotalcite on the changes of esophageal and gastric mucosal ultrastructure in rats induced by WIRS and aspirin. (1) Model of rats with WIRS: SD rats were divided into 2 groups randomly (6 rats per group) and were pretreated with Hydrotalcite (375㎎/㎏/d) or N.S. intragastric administration, in a volume of 2ml seperately, bid, for 4 days. On the 4〓 day, 2 hours after administration all the rats underwent WIRS. After anaesthesia, the Ul of the stomach was measured by Guth's method (scores), and the lower esophageal and gastric mucosal tissues were obtained to measure the intercellular space width (μm) by TEM. (2) Model of rats with aspirin intragastric administration: After 4 days of Hydrotalcite or N.S. intragastric administration, all the rats were treated with aspirin (300㎎/㎏, dissolved in 1ml of 2% NaHCO₃ solution) intragastric administration, once. One hour later, the rats were anesthetized, and the rest procedures were similar to those applied in the model of rats with WIRS. Part Ⅴ: Relationship between the expression leves of cell adhesion molecule CD15 and DIS in the lower esophageal mucosal epithelium. Using method of Western blot, we analyzed the changes of CD15 expression level in the esophageal mucosa of rats from groups of normal controls, N.S. intragastric administration, WIRS and aspirin intragastric administration in Part Ⅰ. Results: Part Ⅰ: Different damaging factors induced erosions and dotted ulcers in rats' gastric mucosa, but produced no gross lesions or histological evidences of cell necrosis or inflammation in the esophageal mucosa, which remained intact. The width of intercellular space within the lower esophageal epithelium in groups of normal controls, N.S. intragastric administration, N.S. hypodermic injection, WIRS, hydrochloric acid intragastric administration, ethanol intragastric administration, aspirin intragastric administration, and prednisolone hypodermic injection were 0.13±0.02 μm, 0.19±0.05 μm, 0.14±0.03 μm, 0.38±0.05 μm, 0.24±0.03 μm, 0.25±0.10 μm, 0.32±0.12 μm and 0.20±0.03 μm respectively. The width of intercellular space in group of WIRS was significantly broader than that in group of normal controls (P<0.01), and the width of intercellular space in group of aspirin intragastric administration were significantly broader than that in group of N.S. intragastric administration (P<0.01). There were no significant differences in the width of intercellular space between the groups of hydrochloric acid intragastric administration and N.S. intragastric administration, ethanol intragastric administration and N.S. intragastric administration, prednisolone hypodermic injection and N.S. hypodermic injection (P>0.05). Part Ⅱ: Pretreatment with esomeprazole has no influence on DIS within the lower esophageal epithelium induced by WIRS or aspirin; there were no significant differences in the width of intercellular space within the lower esophageal mucosal epithelum between the esomeprazole group and N.S. group, whether in model of WIRS or aspirin (0.35±0.05 μm vs. 0.37±0.05 μm, 0.24±0.02 μm vs. 0.27±0.03 μm), P>0.05. Part Ⅲ: In the 4 lesion models, the gastric mucosal UIs were significantly lower in all of the mucosal protective agents groups than that in the N.S. control group (P<0.05). The statistical difference was more significant in the group of Hydrotalcite (P<0.01). The width of the intercellular space within gastric mucosal epithelium in the Hydrotalcite group was significantly narrower than that in the control groups of all the 4 models (P<0.05). Part Ⅳ: Pretreatment with Hydrotalcite has no effect on DIS within the lower esophageal epithelium induced by WIRS or aspirin; there were no significant differences in width of intercellular space within the lower esophageal mucosal epithelium between the Hydrotalcite group and N.S. group, whether in model of WIRS or aspirin (0.34±0.04 μm vs. 0.37±0.05 μm, 0.23±0.01 μm vs. 0.25±0.02 μm), P>0.05. After pretreatment with Hydrotalcite, the gastric mucosal UI and the width of the intercellular space within gastric mucosal epithelium in the Hydrotalcite group were both significantly lower than those of the control group in model of aspirin (4.0±1.4 scores vs. 12.7±5.5 scores, 0.21 ±0.01 μm vs. 0.28±0.01 μm), P<0.05; but there were no significant differences between the Hydrotalcite group and control group whether in the gastric mucosal UI or the width of the intercellular space within gastric mucosal epithelium (9.0±4.1 scores vs. 15.8±7.4 scores, 0.34±0.03 μm vs. 0.37±0.06 μm), P>0.05. Part Ⅴ: The density, band-width and color saturation of CD15 protein bands in the esophageal mucosa of the 4 groups were different, which indicated the differences of CD15 expression level. The level of CD15 protein was higher in groups of normal controls and N.S. intragastric administration, but lower in groups of WIRS and aspirin intragastric administration. After analysis of the bands by GENE GENIUS Bio Imaging system and semi-quantitation sofeware GeneTools, the relative optical density (ROD) of CD15 protein bands in different groups was as follow. The RODs in groups of normal controls and WIRS were 0.32±0.06 and 0.17±0.07 respectively, and there was a significant difference between the two groups (P<0.01); the ROD in group of aspirin intragastric administration was 0.17±0.07, which was significantly lower than that in group of N.S. intragastric administration (0.29±0.06, P<0.01). Conclusions: Ⅰ.WIRS and aspirin can also induce DIS within the lower esophageal mucosal epithelium in the models of gastirc mucosal lesions, and DIS presents before the gross lesion and histological cell necrosis or inflammation in the esophagus. DIS may be an early and sensitive marker of esophageal mucosal damage. Hydrochloric acid, ethanol and prednisolone used in our experiment (including the concentration, dose and action time) have no influence on the width of intercellular space within the lower esophageal mucosal epithelium in the models of gastirc mucosal lesions. Ⅱ.Pretreatment with esomeprazole has no influence on DIS within the lower esophageal mucosal epithelium induced by WIRS or aspirin. WIRS and aspirin induced DIS may have no relationship with acid. Ⅲ. All of the 6 mucosal protective agents have protective effects against the gastric mucosal lesion by ethanol, hydrochloric acid, aspirin and prednisolone. Among them, the protective effect of Hydrotalcite seems even better. The mucosal protective effects of Hydrotalcite were further confirmed according to the observed results of the intercellular space width. Ⅳ.Pretreatment with Hydrotalcite has no effect on DIS within the lower esophageal mucosal epithelium induced by WIRS or aspirin. Hydrotalcite has protective effect against the gastric mucosal lesion by aspirin, and it can reduce the intercellular space width of the gastric mucosal epithelium; but Hydrotalcite has no effect on the gastric mucosal lesion or the intercellular space width of gastric mucosal epithelium in model of WIRS. Ⅴ.The expression level of CD15 protein in groups of WIRS and aspirin were significantly lower than that in groups of normal controls and N.S. controls respectively; the downregulation of CD15 protein, one of the cell adhesion molecules (CAMs), may be correlated with DIS within the lower esophageal mucosal epithelium. [Keywords] esophagus; stomach; mucosal lesions and protection; intercellular space; cell adhesion molecules; CD15

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