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作 者:张盼[1] 张方信[2] 邓芝云[2] 陈嘉屿[2] 单体栋[2]
机构地区:[1]兰州大学第二临床医学院消化科,甘肃兰州730000 [2]兰州军区兰州总医院
出 处:《西北国防医学杂志》2012年第3期210-213,共4页Medical Journal of National Defending Forces in Northwest China
基 金:甘肃省自然科学基金资助项目(1010RJZA052)
摘 要:目的:观察高原缺氧环境下重症急性胰腺炎(severe acute pancreatitis,SAP)大鼠肠黏膜组织的变化,初步探讨高原SAP(H-SAP)时肠黏膜屏障损伤的机制。方法:48只Wistar大鼠,根据海拔不同随机分为2个大组,西安组(X组)和马衔山组(M组),每组24只,再将每个大组随机分为4个小组,假手术组(SO组),SAP-6 h组,SAP-12 h组和SAP-24 h组,每组6只。采用逆行胰胆管注射4%牛磺胆酸钠制备SAP动物模型。分别测定小肠组织TNF-α、IL-10水平;取胰腺及肠组织行病理学检查,透射电镜观察肠黏膜超微结构的变化。结果:X-SAP组与M-SAP组相比,TNF-α、IL-10的表达具有显著性差异(P<0.05);光镜下可见M-SAP组各时间点胰腺及肠组织的损伤程度均较X-SAP组显著(P<0.05);SAP组胰腺组织与肠组织病理评分均呈正相关关系(r=0.902,P<0.01),透射电镜结果显示M-SAP组大鼠造模后肠组织超微结构损伤程度较X-SAP组明显。结论:高原缺氧可诱导、加重H-SAP时肠黏膜屏障损伤;TNF-α和IL-10表达失衡可能在H-SAP合并肠黏膜屏障损伤的发生、发展中起重要作用。Objective:To observe the intestinal mucosal tissue of rats with severe acute pancreatitis (SAP) in platuau hypoxia , and investigate the mechanism of gut barrier injury of rats with SAP at high altitude ( H - SAP). Methods: Forty - eight Wistar rats were randomly divided into 2 groups ( n = 24 for each group), Xihn group (X) and Maxianshan group (M) according to different altitude. Each group was further divided into four subgroups (n =6 for each subgroup), sham -operation group (SO group), SAP -6 h group, SAP - 12 h group and SAP -24 h group, 4% sodium taurocholate was injected into the pancreatic duct to induce SAP. Pancreas and intestine tissues were harvested to observe the pathological changes, ured respectively. The uhrastructure of intestine and the content of TNF - o~ and IL - 10 in intestine were meas- mucosa was observed under transmission electron microscope(TEM). Results:The expression of TNF-or and IL- 10 in X- SAP group was significantly different with that in M - SAP group (P 〈 O. 05 ). Under the light microscopy, injury of pancreas and intestine at different time point in M - SAP group was more obvious than that in X - SAP group ( P 〈 0.05 ). The pathological scores of intestine were positively correlated with that of pancreas in SAP group ( r = 0. 902, P 〈 0.01 ). Injury of intestinal mucosal was more obvious in M -SAP group than that in X- SAP group at each time point under TEM. Conclusion:Injury of intestinal mucosal barrier in rats with SAP can be induced and aggravated in plateau hypoxia. Disturbance of TNF - eL and IL - 10 expression play an important role in the pathogenesis and development of intestinal mucosal barrier injury in rats with H- SAP.
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