Hp感染萎缩性胃炎大鼠模型的建立
发布时间：2018-08-31 16:54
【摘要】：目的：建立较理想的幽门螺杆菌(Hp)感染慢性萎缩性胃炎(CAG)大鼠模型。 方法：采用清洁级、体质量90-110g、雄性Wistar大鼠75只,按每组15只,随机分为模型组(Hp感染及水杨酸钠乙醇灌胃组)、对照A组(正常对照组)、对照B组(单纯Hp感染组)、对照C组(单纯水杨酸钠乙醇灌胃组)、对照D组(去氧胆酸钠乙醇灌胃及氨水自由饮用组)。采用灌胃接种Hp菌株(SS1)及20g/L水杨酸钠与体积分数0.60的乙醇混合溶液灌胃的方法建立Hp感染CAG模型,共14wk。采用Hp细菌培养、胃黏膜涂片革兰染色和快速尿素酶试验检测Hp定植情况,并对胃窦黏膜病理组织学各项指标进行评分。 结果：模型组及对照B组胃窦黏膜均有Hp定植。模型组胃窦黏膜变薄,固有层腺体中度减少伴有中度慢性活动性炎症,未出现肠化生及不典型增生。模型组慢性炎症评分、活动性炎症评分及固有腺减少评分(依次为2.03±0.18,0.68±0.11,2.05±0.19)均明显高于对照A组及对照B组(依次为0.16±0.05,0.15±0.05,0；0.39±0.11,0.30±0.08,0；q=6.514-11.191,P0.01),与对照C组及对照D组(依次为1.95±0.19,。0.54±0.08,2.02±0.19；1.80±0.14,0.45±0.09,1.92±0.18)比较,差异无显著性(q=0.618-2.439,P0.05)。 结论：采用Hp感染大鼠及水杨酸钠乙醇混合溶液灌胃的综合方法建立Hp感染CAG大鼠模型,其病因、病理变化与人类CAG病变相似,可作为研究Hp感染CAG发病机制及药物干预治疗CAG较合适的动物模型。
[Abstract]:Objective: to establish an ideal (CAG) rat model of Helicobacter pylori (Hp) infection with chronic atrophic gastritis. Methods: Seventy-five male Wistar rats with body mass 90-110 g were used in each group, 15 rats in each group. Model group (Hp infection and sodium salicylate ethanol), control group A (normal control group), control group B (simple Hp infection group), control group C (sodium salicylate alcohol infusion group), control group D (deoxycholic acid) Sodium ethanol and ammonia free drinking group). The CAG model of Hp infection was established by intragastric administration of Hp strain (SS1) and 20g/L sodium salicylate and ethanol mixed solution with volume fraction of 0.60 for 14 wk. Hp bacteria culture, gastric mucosal smear Gram staining and rapid urease test were used to detect the colonization of Hp, and the histopathological indexes of gastric antral mucosa were evaluated. Results: Hp colonization was found in antral mucosa of model group and control group. In the model group, gastric antral mucosa became thinner, the gland of lamina propria decreased moderately with moderate chronic active inflammation, no intestinal metaplasia or atypical hyperplasia occurred. The scores of chronic inflammation, active inflammation and reduction of intrinsic gland in the model group (2.03 卤0.18 卤0.68 卤0.112.05 卤0.19) were significantly higher than those in the control group A and B (0.16 卤0.05 卤0.15 卤0.05U 0.39 卤0.110.30 卤0.08q6.514-11.191P0.01, respectively), as compared with those in the control group C and group D (1.95 卤0.19.19.0.54 卤0.082.02 卤0.1982.02 卤0.191.80 卤0.140.45 卤0.091.92 卤0.18). There was no significant difference (P 0.05). Conclusion: the model of CAG rats infected with Hp and sodium salicylate alcohol was established by the method of intragastric instillation of Hp and sodium salicylate ethanol mixed solution. The etiology and pathological changes of CAG rats were similar to those of human CAG. It can be used as a more suitable animal model to study the pathogenesis of Hp infection of CAG and to treat CAG with drug intervention.
【学位授予单位】：青岛大学
【学位级别】：硕士
【学位授予年份】：2012
【分类号】：R-332;R573.3
本文编号：2215588
[Abstract]:Objective: to establish an ideal (CAG) rat model of Helicobacter pylori (Hp) infection with chronic atrophic gastritis. Methods: Seventy-five male Wistar rats with body mass 90-110 g were used in each group, 15 rats in each group. Model group (Hp infection and sodium salicylate ethanol), control group A (normal control group), control group B (simple Hp infection group), control group C (sodium salicylate alcohol infusion group), control group D (deoxycholic acid) Sodium ethanol and ammonia free drinking group). The CAG model of Hp infection was established by intragastric administration of Hp strain (SS1) and 20g/L sodium salicylate and ethanol mixed solution with volume fraction of 0.60 for 14 wk. Hp bacteria culture, gastric mucosal smear Gram staining and rapid urease test were used to detect the colonization of Hp, and the histopathological indexes of gastric antral mucosa were evaluated. Results: Hp colonization was found in antral mucosa of model group and control group. In the model group, gastric antral mucosa became thinner, the gland of lamina propria decreased moderately with moderate chronic active inflammation, no intestinal metaplasia or atypical hyperplasia occurred. The scores of chronic inflammation, active inflammation and reduction of intrinsic gland in the model group (2.03 卤0.18 卤0.68 卤0.112.05 卤0.19) were significantly higher than those in the control group A and B (0.16 卤0.05 卤0.15 卤0.05U 0.39 卤0.110.30 卤0.08q6.514-11.191P0.01, respectively), as compared with those in the control group C and group D (1.95 卤0.19.19.0.54 卤0.082.02 卤0.1982.02 卤0.191.80 卤0.140.45 卤0.091.92 卤0.18). There was no significant difference (P 0.05). Conclusion: the model of CAG rats infected with Hp and sodium salicylate alcohol was established by the method of intragastric instillation of Hp and sodium salicylate ethanol mixed solution. The etiology and pathological changes of CAG rats were similar to those of human CAG. It can be used as a more suitable animal model to study the pathogenesis of Hp infection of CAG and to treat CAG with drug intervention.
【学位授予单位】：青岛大学
【学位级别】：硕士
【学位授予年份】：2012
【分类号】：R-332;R573.3
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