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门静脉高压性胃病小鼠模型的建立
引用本文:李鹏,李扬,谭嗣伟,刘慧玲,吴斌.门静脉高压性胃病小鼠模型的建立[J].新医学,2012,43(5):318-321,F0002.
作者姓名:李鹏  李扬  谭嗣伟  刘慧玲  吴斌
作者单位:1. 中山大学附属第一医院病理科,510080
2. 中山大学附属第三医院消化科,510630
基金项目:国家自然科学基金,广东省科技计划重点项目
摘    要:目的:建立门静脉高压性胃病(PHG)小鼠模型;检测PHG小鼠胃黏膜细胞凋亡和活化Caspase-3表达情况。方法:分别采用部分缩窄门静脉联合左肾上腺静脉结扎(PPVL+LAVL)、腹腔注射四氯化碳建立C57BL/6小鼠门静脉高压模型(32只小鼠随机分为4组,包括假手术组、PPVL+LAVL组以及对照组、四氯化碳组),测量门静脉压力,进行肝胃组织苏木素-伊红染色、TUNEL标记检测染色计算凋亡指数、免疫组织化学检测活化Caspase-3表达情况,比较各组结果。结果:与假手术组相比,PPVL+LAVL组门静脉压力高(9.5±0.8)mm Hg对比(5.9±0.4)mm Hg,P<0.01],凋亡指数高(9.2±0.9对比0.7±0.3,P<0.01),胃组织损害明显;与对照组相比,四氯化碳组肝组织呈中重度肝纤维化,门静脉压力高(8.8±0.9)mm Hg对比(6.1±0.5)mm Hg,P<0.01],凋亡指数高(8.2±1.9对比1.9±0.6,P<0.01),胃组织出现损害。PPVL+LAVL组和四氯化碳组小鼠胃黏膜活化Caspase-3表达明显增多。结论:该研究成功建立两种小鼠PHG模型;PHG小鼠胃黏膜细胞凋亡增多,活化Caspase-3表达增多。

关 键 词:门静脉高压性胃病  凋亡  胃黏膜细胞  小鼠

Establishment of portal hypertensive gastropathy model in mice
LI Peng , LI Yang , TAN Si-wei , LIU Hui-ling , WU Bin.Establishment of portal hypertensive gastropathy model in mice[J].New Chinese Medicine,2012,43(5):318-321,F0002.
Authors:LI Peng  LI Yang  TAN Si-wei  LIU Hui-ling  WU Bin
Institution:1 Department of Pathology, The First Affiliated Hospital, SUN Yat-sen University, Guangzhou 510080, China; 2 Department of Gastroenterology, The Third Affiliated Hospital, SUN Yat-sen University, Guangzhou 510630, China )
Abstract:Objective: To establish the portal hypertensive gastropathy model in mice and to further investigate the apoptosis and the expression of cleaved Caspase-3 in gastric tissues of mice with portal hypertensive gastropathy. Methods: Thirty-two mice were randomly divided into 4 groups (partial portal vein ligation plus left adrenal vein ligation (PPVL + LAVL) group, CCl4 group, sham operation group and control group). Portal hypertension models were established by partial portal vein ligation plus left adrenal vein ligation ( PPVL + LAVL), and by intraperitoneal injection of carbon tetrachloride ( CCI4), respectively. Portal pressures were measured. HE staining was applied pathological observation of hepatic and gastric tissues. Apoptosis index and cleavage Caspase-3 expression were assessed via TUNEL and immunohistochemistry, respectively. Results: Comparing with sham operation group, significantly higher portal pressure (9.5 ±0. 8) mm Hg vs (5.9±0. 4) mm Hg, P 〈0. 01 ], higher ap- optosis index (9.2 ± 0. 9 vs. 0. 7 - 0. 3, P 〈 0. 01 ), and more prominent gastric mucosa injury were observed in PPVL + LAVL group. Comparing with control group, moderate-severe hepatic fibrosis, significantly higher portal pressure (8.8±0.9) mm Hg vs (6.1 ±0. 5) mm Hg, P〈0.01], and higher apoptosis index (8.2 ±1.9 vs. 1.9±0. 6, P 〈0. 01) were revealed i.n CCI4 group with some gastric mucosa impairment. The expression of cleaved Caspase-3 was significantly increased in PPVL + LAVL and CCI4 group. Conclusion: Two portal hypertensive gastropathy models in mice were established. Elevated apoptosis and expression of cleaved Caspase-3 are observed in portal hypertensive gastropathy mice.
Keywords:Portal hypertensive gastropathy  Apoptosis  Gastric mucosa cell  Mice
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