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作 者:黄继义[1] 刘才文[1] 林建东[2] 叶先龙[1] 洪朝基 周荣[4]
机构地区:[1]厦门大学附属第一医院同民分院内科,福建厦门361000 [2]福建医科大学附属第一医院ICU [3]福建省厦门医科所内科 [4]厦门大学附属第一医院急诊科
出 处:《西南国防医药》2014年第1期23-26,共4页Medical Journal of National Defending Forces in Southwest China
摘 要:目的探讨TOLL样受体4(TLR-4)表达对脂多糖诱导急性肺损伤(ALI)大鼠体内炎症因子的影响,明确阻断TLR-4表达对急性肺损伤的保护作用。方法 45只雄性Wistar大鼠随机分为:正常对照组、ALI组和干预组,每组15只。ALI组和干预组采用静脉注射脂多糖(LPS)方法构建急性肺损伤模型,对照组注射等量的生理盐水。各组动物再按照观察时间点平均分为造模后6、12和24 h各3个亚组。测定各组肺组织TLR-4 mRNA表达以及支气管肺泡灌洗液中炎症因子浓度,观察各组大鼠肺组织的病理变化。结果 LPS可以导致肺泡腔内TNF-α、IL-1β和IL-6浓度增加,阻断TLR-4受体会抑制炎症因子释放;ALI组的肺损伤评分高于干预组和正常对照组(3.3±1.1 vs.1.9±1.0 vs.1.2±0.9)。结论阻断TLR-4表达能抑制脂多糖诱导ALI大鼠体内炎症因子分泌,减轻肺组织病理损害,能达到治疗ALI的作用。Objective To discuss the effects of Toll-like receptor(TLR)4 expression on the inflammatory factors in rats with acute lung injury induced by lipopolysaccharide, and to explore the protection effect of blocking the TLR-4 expression on acute lung injury. Methods Forty five male Wistar rats were randomly divided into normal control group, ALI group, and intervention group with 15 ones in each group. In ALI and intervention groups, the models of acute lung injury were established by the method of intravenous injection with lipopolysaccharide(LPS). The control group received the injection with the same volume of normal saline. All the animals were divided into subgroups of 6,12, and 24 h according to the observation timing of the modeling. Detection was made in the TLR-4 mRNA expression in the lung tissues of those animals and the concentration of the inflammatory factors in the bronchoalveolar lavage fluid. The pathological changes in the rats'lung tissues were observed. Results LPS could lead to the increase of TNF-a, IL-Iβ, and IL- 6 in alveolar space. Blocking the TLR-4 receptor could inhibit the release of inflammatory factors. The evaluation score of lung injury in ALl group was higher than those in the intervention and normal control group (3.3 ± 1.1 vs. 1.9 ± 1.0 vs. 1.2 ± 0.9). Conclusion Blocking TLR-4 expression can inhibit the secretion of inflammatory factor in ALI rats model induced by LPS, relieve the pathological lesion of lung tissues, and cure ALI.
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