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机构地区:[1]首都医科大学附属北京同仁医院消化内科,北京市100730
出 处:《世界华人消化杂志》2009年第8期813-816,共4页World Chinese Journal of Digestology
摘 要:目的:探讨选择性诱导型一氧化氮合酶抑制剂氨基胍(aminoguanidine,AG)对肝硬化大鼠门脉高压性胃黏膜病变的防治作用及其机制.方法:将SD大鼠30只随机分为对照组(n=10)、模型组(n=10)和AG组(n=10),予400mL/LCCl4皮下注射12wk建立肝硬化大鼠模型,AG组为皮下注射CCl4同时予AG饮用.观察比较各组大鼠胃黏膜形态及组织学变化,应用免疫组化法检测胃黏膜诱导型一氧化氮合酶(iNOS)的表达,并测定胃黏膜溃疡指数、门静脉压力.结果:AG组胃黏膜病变程度较模型组减轻,溃疡指数明显低于模型组(3.00±2.31vs10.60±3.47,P<0.01);模型组胃黏膜iNOS吸光度、面密度值均较对照组增高(0.64±0.04vs0.25±0.03;0.344±0.068vs0.017±0.008,均P<0.01),AG组胃黏膜iNOS吸光度值、面密度值(0.46±0.09,0.159±0.021)均较模型组明显下降(均P<0.01).AG组门脉压力较模型组降低.结论:AG可在一定程度上减轻门脉高压性胃黏膜病变,其机制可能主要通过抑制胃黏膜iNOS表达.AIM: To investigate the effect and mechanism of aminoguanidine (AG) on the portal hypertensive gastropathy in cirrhotic rats. METHODS: Thirty male SD rats were randomly divided into three groups: control group (n = 10), model group (n = 10) and AG treatment group (n = 10) (AG group). The model group was induced through subcutaneous injection of CCl4 for 12 weeks, AG group was given subcutaneous injection of CCl4 together with oral administration of AG. The morphological and histological changes in gastric mucosa were evaluated. The expres- sion of iNOS in gastric mucosa was detected by SABC immunohistochemical methods. And the ulcer-index (UI) of gastric mucosa, and portal pressure were measured in each group. RESULTS: Histological changes of gastric mu-cosa was milder and ulcer index of gastric mucosa was significantly lower in AG group than in model group (3.00 ± 2.31 vs 10.60 ±3.47, P 〈 0.01). The expression of iNOS (optical density and area density) in gastric mucosa was signifi cantly higher in model group than in control group (0.64 ± 0.04 vs 0.25 ± 0.03; 0.344 ± 0.068 vs 0.017 ± 0.008, both P 〈 0.01). Optical density and area density were significantly lower in AG group than in model group (0.46 ±0.09 vs 0.64 ± 0.04; 0.159 ± 0.021 vs 0.344 ± 0.068, both P 〈 0.01), and the portal pressure were lower in AG group than in model group. CONCLUSION: Aminoguanidine may ame- liorate the development of portal hypertensive gastropathy through significantly inhibiting the expression of iNOS in gastric mucosa.
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