Hp感染萎縮性胃炎大鼠模型的建立
發(fā)布時間：2018-08-31 16:54
【摘要】：目的：建立較理想的幽門螺桿菌(Hp)感染慢性萎縮性胃炎(CAG)大鼠模型。 方法：采用清潔級、體質(zhì)量90-110g、雄性Wistar大鼠75只,按每組15只,隨機分為模型組(Hp感染及水楊酸鈉乙醇灌胃組)、對照A組(正常對照組)、對照B組(單純Hp感染組)、對照C組(單純水楊酸鈉乙醇灌胃組)、對照D組(去氧膽酸鈉乙醇灌胃及氨水自由飲用組)。采用灌胃接種Hp菌株(SS1)及20g/L水楊酸鈉與體積分數(shù)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細菌培養(yǎng)、胃黏膜涂片革蘭染色和快速尿素酶試驗檢測Hp定植情況,并對胃竇黏膜病理組織學(xué)各項指標進行評分。 結(jié)果：模型組及對照B組胃竇黏膜均有Hp定植。模型組胃竇黏膜變薄,固有層腺體中度減少伴有中度慢性活動性炎癥,未出現(xiàn)腸化生及不典型增生。模型組慢性炎癥評分、活動性炎癥評分及固有腺減少評分(依次為2.03±0.18,0.68±0.11,2.05±0.19)均明顯高于對照A組及對照B組(依次為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),與對照C組及對照D組(依次為1.95±0.19,。0.54±0.08,2.02±0.19；1.80±0.14,0.45±0.09,1.92±0.18)比較,差異無顯著性(q=0.618-2.439,P0.05)。 結(jié)論：采用Hp感染大鼠及水楊酸鈉乙醇混合溶液灌胃的綜合方法建立Hp感染CAG大鼠模型,其病因、病理變化與人類CAG病變相似,可作為研究Hp感染CAG發(fā)病機制及藥物干預(yù)治療CAG較合適的動物模型。
[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 鹵0.18 鹵0.68 鹵0.112.05 鹵0.19) were significantly higher than those in the control group A and B (0.16 鹵0.05 鹵0.15 鹵0.05U 0.39 鹵0.110.30 鹵0.08q6.514-11.191P0.01, respectively), as compared with those in the control group C and group D (1.95 鹵0.19.19.0.54 鹵0.082.02 鹵0.1982.02 鹵0.191.80 鹵0.140.45 鹵0.091.92 鹵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.
【學(xué)位授予單位】：青島大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2012
【分類號】：R-332;R573.3
本文編號：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 鹵0.18 鹵0.68 鹵0.112.05 鹵0.19) were significantly higher than those in the control group A and B (0.16 鹵0.05 鹵0.15 鹵0.05U 0.39 鹵0.110.30 鹵0.08q6.514-11.191P0.01, respectively), as compared with those in the control group C and group D (1.95 鹵0.19.19.0.54 鹵0.082.02 鹵0.1982.02 鹵0.191.80 鹵0.140.45 鹵0.091.92 鹵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.
【學(xué)位授予單位】：青島大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2012
【分類號】：R-332;R573.3
【參考文獻】
相關(guān)期刊論文 前4條
1 張鳳娟;江月萍;趙清喜;;幽門螺桿菌vacA及cagA基因型與胃疾病的關(guān)系[J];青島大學(xué)醫(yī)學(xué)院學(xué)報;2010年02期
2 金東明,吳巍,孫樹權(quán),齊忠志,董沛生,趙振剛;改良半夏瀉心湯治療慢性萎縮性胃炎實驗研究[J];長春中醫(yī)學(xué)院學(xué)報;2001年03期
3 李秋娟,仲來福,葉建新,宋淑云;大鼠實驗性慢性萎縮性胃炎與胃粘膜生長抑素、胃泌素關(guān)系的研究[J];大連醫(yī)科大學(xué)學(xué)報;1999年02期
4 陳小野,鄒世潔,樊雅莉,張宇鵬;大鼠慢性萎縮性胃炎證病結(jié)合模型胃粘膜病理研究[J];上海實驗動物科學(xué);2002年01期
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