肠缺血再灌注损伤大鼠小肠运动功能的变化与细胞间黏附分子1表达的关系

Objective To evaluate the relationship between the intestinal motility alterations and intercellular adhesion molecule-1 ( ICAM-1 ) expression within the rat intestinal muscularis after ischemia reperfusion. Methods Thirty Wistar rats were divided randomly into IIR, monoclanal anti-ICAM-1 and sham group (n = 10), HR models were established by clamping-releasing the superior mesenteric artery. Gut transit was measured in vivo and intestinal circular muscle contractions were measured in an organ bath. The expression of ICAM-1 mRNA was detected by RT-PCR and immunohistochemisty. Leukocyte infiltration and myeloperoxidase (MPO) activity were quantified in sham and ischemia/reperfusion rats with and without monoclonal anti-ICAM-1 antibody treatment. Results The gut transit of monoclonal anti-ICAM-1 group was improved obviously as compared with IIR group. Circular smooth muscle contractility stimulated by ICAM-1 mRNA expression was 1.69 ± 0. 57 and 1.76 ± 0. 32 within the muscularis; Leukocyte infiltration into the muscularis was (5.6 ±2. 2) c/f and ( 18. 2 ±3. 1 ) c/f. MPO activity was (2. 03 ±0. 56) U/g and (6. 41 ± 1.25 ) U/g respectively. The differences were all statistically significant between IIR and treatment groups ( P ＜ 0. 05 ). The expression of ICAM-1 protein in IIR and anti-ICAM-1 groups was not significantly different (P ＞ 0. 05). Conclusions The up-regulated expression of ICAM-1 after ⅡR injury calls forth local infiltration of PMN within the intestinal muscularis, leading to intestinal motility dysfunction.     

慢性胰腺炎大鼠肝组织NF—κB的表达及中药的干预作用

目的:研究实验性慢性胰腺炎大鼠肝组织核转录因子(NF-κB)的表达以及药物的干预作用。方法:建立慢性胰腺炎大鼠模型,Western印迹法检测各组大鼠肝组织NF-κB蛋白的表达,应用放免法检测血清IL-6、TNF-α的水平。结果:慢性胰腺炎模型组大鼠肝组织NF-κB蛋白的表达较对照组明显升高(P<0.05),且血清细胞因子IL-6、TNF-α含量增加。大承气颗粒治疗组及丹参治疗组NF-κB的表达较模型组明显降低(P<0.05)。结论:慢性胰腺炎导致大鼠肝组织NF-κB蛋白的表达升高,大承气颗粒及丹参对NF-κB蛋白的表达有明显的抑制作用。     

胃脂肪肉瘤并溃疡出血一例

患者女,53岁.主因上腹部胀满不适半个月,黑便伴乏力5 d于2005年3月9日入院.既往史：14年前行胆囊切除术,1年前行子宫和双附件切除.入院查体：轻度贫血貌,全身浅表淋巴结无肿大,全腹无压痛,未扪及肿块,无移动性浊音.     

去肝脏胆碱能神经大鼠模型的建立与评价

目前去肝脏胆碱能神经动物模型尚没有明确标准 ,只能通过仔细操作确保肝脏与食道及贲门之间没有组织残留[1] 。我们建立了去肝脏胆碱能神经(IHCD)大鼠模型的手术规范 ,从形态学、免疫组织化学以及超微结构等角度对这一模型进行了全面的评价。一、材料和方法1.实验动物与分组 :健康Wistar大鼠 2 8只 ,体重 170～ 2 0 0 g(购自军事医学科学院第四研究所 ) ,随机分为模型组和对照组 ,每组 14只。2 .模型制备方法 :参照Tordoff等[2 ]的方法 ,加以改进 ,使肝脏完全游离。大鼠禁食不禁水 12h ,10 %水合氯醛腹腔注射麻醉 (3 0 0mg/kg体重 ) ,腹…     

油酸诱导慢性胰腺炎大鼠肝脏细胞GLUT2蛋白表达的改变

目的建立油酸诱导的慢性胰腺炎（chronic pancreatitis,CP）大鼠模型,观察其肝脏葡萄糖载体2（glucose transporter-2,GLUT2）蛋白表达的改变,探讨慢性胰腺炎继发性糖代谢异常的可能机制。方法用油酸经胰胆管插管灌注的方法诱导CP大鼠模型,对照组大鼠经插管灌注等量生理盐水,Western blot法测定各组大鼠肝细胞GLUT2蛋白表达的改变。结果模型组GLUT2蛋白的表达较对照组都有明显降低（P〈0．05）。结论慢性胰腺炎时GLUT2蛋白表达降低,导致胰岛素信号转导异常,这可能是CP继发糖代谢异常的机制之一。     

慢性胰腺炎大鼠肝组织NF-кB的表达及中药的干预作用

目的:研究实验性慢性胰腺炎大鼠肝组织核转录因子(NF-кB)的表达以及药物的干预作用.方法:建立慢性胰腺炎大鼠模型,Western印迹法检测各组大鼠肝组织NF-кB蛋白的表达,应用放免法检测血清IL-6、TNF-α的水平.结果:慢性胰腺炎模型组大鼠肝组织NF-к蛋白的表达较对照组明显升高(P<0.05),且血清细胞因子IL-6、TNF-α含量增加.大承气颗粒治疗组及丹参治疗组NF-кB的表达较模型组明显降低(P<0.05).结论:慢性胰腺炎导致大鼠肝组织NF-кB蛋白的表达升高,大承气颗粒及丹参对NF-кB蛋白的表达有明显的抑制作用.     

迷走神经对大鼠肝脏葡萄糖代谢和纤维化的影响

目的:研究迷走神经对于大鼠肝脏葡萄糖代谢和肝纤维化形成的影响。方法:（1）建立去迷走神经肝脏模型,SD大鼠32只分模型组及对照组,每组16只。模型组切除迷走神经肝支,对照组仅行开腹神经探查手术。术后每周各采集1次肝脏组织标本,每次4只,连续4周。标本进行VAChT免疫组化,观察肝脏胆碱能神经纤维的表达情况。（2）肝糖原及肝纤维化指标测定.SD大鼠32只分为实验空腹、实验进食及对照空腹和对照进食4组,各8只。实验组行迷走神经肝支切除,对照组行开腹神经探查手术。各组分别测定肝糖原,以及肝组织HA、LN、PC Ⅲ和CIV含量。结果:模型组去迷走神经3周后肝胆碱能神经明显减少,第4周基本消失。实验组空腹肝糖原含量显著低于对照组（P<0.01）,且进食后亦无明显变化（P<0.05）,而对照组进食后肝糖原增加显著（P<0.01）。实验组HA、LN、PC Ⅲ和CIV含量明显高于对照组（P<0.01或P<0.05）。结论:大鼠去除迷走神经后4周,能够达到完全去神经肝脏状态,肝脏去迷走神经后葡萄糖的合成和储存能力显著降低,去神经后肝脏的抗纤维化能力明显减弱。     

胰岛素受体及其信号传递

胰岛β细胞分泌的胰岛素是一种双链多肽的蛋白质激素,它在促进细胞增殖、分化以及蛋白质、脂肪、糖原的合成代谢中发挥重要作用。它促进细胞摄取葡萄糖、氨基酸及脂肪酸、促进糖原、蛋白质     

油酸诱导慢性胰腺炎大鼠肝脏细胞IR及IRS-1蛋白表达的改变

目的:观察慢性胰腺炎(CP)模型大鼠肝脏胰岛素受体(IR),胰岛素受体底物-1(IRS-1)蛋白表达的改变,探讨慢性胰腺炎继发性糖代谢异常的可能机制。方法:将用油酸诱导的CP大鼠作为模型组,同法注入生理盐水的大鼠为对照组,Western blot法测定各组大鼠肝细胞IR,IRS-1蛋白表达的改变。结果:模型组IR,IRS-1蛋白的表达较对照组都有明显降低(P<0.05)。结论:胰岛素信号转导异常可能参与了CP继发糖代谢异常的机制。     

肠缺血再灌注损伤大鼠小肠运动功能的变化与细胞间黏附分子1表达的关系

Objective To evaluate the relationship between the intestinal motility alterations and intercellular adhesion molecule-1 ( ICAM-1 ) expression within the rat intestinal muscularis after ischemia reperfusion. Methods Thirty Wistar rats were divided randomly into IIR, monoclanal anti-ICAM-1 and sham group (n = 10), HR models were established by clamping-releasing the superior mesenteric artery. Gut transit was measured in vivo and intestinal circular muscle contractions were measured in an organ bath. The expression of ICAM-1 mRNA was detected by RT-PCR and immunohistochemisty. Leukocyte infiltration and myeloperoxidase (MPO) activity were quantified in sham and ischemia/reperfusion rats with and without monoclonal anti-ICAM-1 antibody treatment. Results The gut transit of monoclonal anti-ICAM-1 group was improved obviously as compared with IIR group. Circular smooth muscle contractility stimulated by ICAM-1 mRNA expression was 1.69 ± 0. 57 and 1.76 ± 0. 32 within the muscularis; Leukocyte infiltration into the muscularis was (5.6 ±2. 2) c/f and ( 18. 2 ±3. 1 ) c/f. MPO activity was (2. 03 ±0. 56) U/g and (6. 41 ± 1.25 ) U/g respectively. The differences were all statistically significant between IIR and treatment groups ( P ＜ 0. 05 ). The expression of ICAM-1 protein in IIR and anti-ICAM-1 groups was not significantly different (P ＞ 0. 05). Conclusions The up-regulated expression of ICAM-1 after ⅡR injury calls forth local infiltration of PMN within the intestinal muscularis, leading to intestinal motility dysfunction.