α, IL-1β, and NO) and antiinflammatory (IL-10, CO) levels were assayed in serum, liver, and small bowel in order to verify a hypothetic inflammatory etiopathogeny of portal hypertension that could be the cause of its evolutive heterogeneity. Male Wistar rats were divided into one control group (n=11) and one group with a triple stenosing ligation of the portal vein (n=23) after 28 days of evolution. In one subgroup of portal hypertensive rats, portal pressure, collateral venous circulation, mesenteric vasculopathy, and liver and spleen weights were determined. In the remaining rats with portal hypertension TNF-α, IL-1β, and IL-10 were quantified in liver and ileum by enzyme-linked immunosorbent assay. NO synthase activity was studied in liver and ileum. CO and NO were measured in portal and systemic blood by spectrophotometry and Griess reaction, respectively. Portal hypertensive rats with mayor spleen weight show hepatomegaly and mayor development of collateral circulation. Ileum release of IL-10 (0.30±0.12 versus 0.14±0.02 pmol/mg protein; P<.01) is associated with a liver production of both proinflammatory mediators (TNF-α: 2±0.21 versus 1.32±0.60 pmol/mg protein; P<.05, IL-1β: 19.17±2.87 versus 5.96±1.84pmol/mg protein; P=.005, and NO: 132.10±34.72 versus 61.05±8.30nmol/mL; P=.005) and an antiinflammatory mediator (CO: 6.49±2.99 versus 3.03±1.59pmol/mL; P=.005). In short-term prehepatic portal hypertension a gut-liver inflammatory loop, which could be fundamental in the regulation both of the portal pressure and of its complications, could be proposed."> 门脉高压大鼠的促炎性肝脏和抗炎性肠道介质 - raybet雷竞app,雷竞技官网下载,雷电竞下载苹果
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2005 |物品ID 387427 | https://doi.org/10.1155/MI.2005.101

玛丽亚·安吉尔·阿勒、埃琳娜·瓦拉、克鲁兹·加西亚、玛丽亚·多洛雷斯·帕尔马、豪尔赫·阿里亚斯、玛丽亚·帕斯·纳瓦、詹姆·阿里亚斯, "门脉高压大鼠的促炎性肝脏和抗炎性肠道介质",炎症介质, 卷。2005, 物品ID387427, 11 , 2005. https://doi.org/10.1155/MI.2005.101

门脉高压大鼠的促炎性肝脏和抗炎性肠道介质

收到 2004年11月17日
认可的 2004年12月17日

摘要

促炎(TNF- α ,IL-1 β 检测血清、肝脏和小肠中的NO)和抗炎(IL-10,CO)水平,以验证门静脉高压症的假定炎症病因,该病因可能是其进化异质性的原因。雄性Wistar大鼠分为一个对照组( N = 11 )一组行门静脉三重狭窄结扎术( N = 23 )在一组门静脉高压症大鼠中,测定门静脉压力、侧支静脉循环、肠系膜血管病变以及肝脏和脾脏重量。在其余的门静脉高压症大鼠中,测定TNF- α ,IL-1 β 通过酶联免疫吸附试验测定肝脏和回肠中的IL-10和NO,研究肝脏和回肠中的NO合酶活性,通过分光光度法和Griess反应分别测定门静脉和全身血液中的CO和NO。脾脏重量较大的门静脉高压大鼠显示肝脏肿大和主要侧支发育l循环。回肠释放IL-10( 0.30 ± 0.12 0.14 ± 0.02  pmol / 蛋白质; P < .01 )与肝脏产生两种促炎症介质(TNF)有关- α : 2. ± 0.21 1.32 ± 0.60  pmol / 蛋白质; P < .05 ,IL-1 β : 19.17 ± 2.87 5.96 ± 1.84 pmol / 蛋白质; P = .005 ,而编号: 132.10 ± 34.72 61.05 ± 8.30 nmol / 毫升 ; P = .005 )和一种抗炎介质(CO: 6.49 ± 2.99 3.03 ± 1.59 pmol / 毫升 ; P = .005 )在短期肝前型门静脉高压症中,可以提出一种肠-肝炎症循环,它可能是调节门静脉压力及其并发症的基础。

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