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目的 利用Hp感染的Wistar大鼠模型进行实验性胃癌研究 ,观察Hp感染是否增加腺胃粘膜对致癌剂的敏感性 ,促进肿瘤形成。方法 2级 ,雄性Wistar大鼠 90只 ,随机分为实验组 (45只 )和对照组 (45只 )。实验组动物感染Hp后 12周 ,将两组动物又随机分为 3小组 ,即空白组、MNNG组和MNNG +NaCl组 ,各 15只。空白组动物自由饮用蒸馏水 ,MNNG组动物饮用含MNNG 10 0 μg/ml的蒸馏水 ,MNNG +NaCl组动物除饮用含MNNG10 0 μg/ml的蒸馏水外 ,另外灌喂 10 %NaCl溶液 1 5ml,2次 /周 ;以上处理连续 10个月 ,处理因素结束后 2个月处死动物。比较各组动物腺胃粘膜病理组织学差异。结果 所有实验组动物至实验结束Hp检查均为阳性。在实验组中的MNNG +NaCl组有 1只动物出现早期腺胃癌。实验组中的MNNG组和MNNG +NaCl组动物腺胃粘膜腺瘤样增生的发生率分别为 4 0 %、5 7 14 % ,显著高于相应的对照组动物的 6 6 7%、15 38% (P <0 0 5 )。在实验组中的空白组、MNNG组和MNNG +NaCl组动物胃窦萎缩性胃炎发生率分别为 6 6 6 7%、80 %和 85 71% ,高于相应的对照组动物的 0 %、2 0 %和 2 3 0 8% (P <0 0 1)。结论 本研究结果提示Hp感染可增加腺胃粘膜对致癌剂的敏感性 ,促进胃癌前病变的形成
OBJECTIVE: To investigate whether Hp infection can increase the sensitivity of glandular gastric mucosa to carcinogens and promote tumor formation by using Hp infected Wistar rat model. Methods Totally 90 male Wistar rats were randomly divided into experimental group (n = 45) and control group (n = 45). Twelve weeks after experimental group infected with Hp, the two groups of animals were randomly divided into three groups: blank group, MNNG group and MNNG + NaCl group, 15 rats in each group. Animals in the blank group were allowed to drink distilled water. MNNG animals were given distilled water containing MNNG 10 0 μg / ml. MNNG + NaCl group were given distilled water containing MNNG10 0 μg / ml, 15 ml of 10% NaCl solution, / Week; the above treatment for 10 consecutive months, two months after the completion of treatment factors animals were sacrificed. The histopathological changes of gland mucosa in each group were compared. Results All experimental animals were positive for Hp test at the end of the experiment. One animal in the MNNG + NaCl group in the experimental group had early gastric adenocarcinoma. In the experimental group, the incidences of gastric glandular adenomatous hyperplasia in MNNG group and MNNG + NaCl group were 40% and 5714%, respectively, which were significantly higher than those in the corresponding control group (66.7% and 15.38% (P <0 05). The incidences of antral gastritis in the blank group, MNNG group and MNNG + NaCl group were respectively 6 6 6 7%, 80% and 85 71% in the experimental group, which were higher than those in the corresponding control group 0%, 2 0% and 230% (P <0.01). Conclusion The results of this study suggest that Hp infection can increase the sensitivity of glandular gastric mucosa to carcinogens and promote the formation of gastric precancerous lesions