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机构地区:[1]南京军区福州总医院医务部,福州医学博士350025 [2]南京军区福州总医院急诊科,福州350025
出 处:《医学研究生学报》2011年第1期25-28,共4页Journal of Medical Postgraduates
摘 要:目的热应激(heat stress)是机体暴露在热环境中产生的一系列非特异性全身反应,多种细胞因子在热应激发生发展的病理过程起重要作用。文中探讨热应激大鼠早期外周血中细胞因子TNF-α、IL-1、IL-6、IL-10的表达及蛋白酶抑制剂乌司他丁(ulinastatin)对热应激的干预作用。方法将SD大鼠随机分为3组:正常对照组、热应激组、乌司他丁干预组,每组10只。热应激组、乌司他丁干预组均建立热应激大鼠模型,各组在6、12、24 h后取动脉血标本,用ELISA法测定TNF-α、IL-1、IL-6、IL-10水平,同时记录体温、心率、动脉收缩压(systolic arterial pressure,SAP)和呼吸频率。结果热应激组大鼠各时间点血清TNF-α、IL-1、IL-6、IL-10水平均高于正常对照组(P<0.01),其中IL-10水平在各时间点逐渐降低。乌司他丁干预组大鼠各时间点血清TNF-α、IL-1、IL-6水平均低于热应激组(P<0.01),而IL-10水平在各时间点均高于热应激组(P<0.01)。乌司他丁干预组大鼠体温、心率、呼吸频率均低于热应激组(P<0.01)。结论热应激大鼠在24 h内促炎细胞因子水平明显增加,全身炎症反应明显,24 h后促炎细胞因子水平呈下降趋势。乌司他丁早期干预可降低TNF-α、IL-1、IL-6水平,提高IL-10水平,具有双相调节作用。Objective Heat stress is a series of non-specific systemic reactions induced by exposure to thermal environment.Various cytokines may play important roles in the pathogenesis and development of heat stress.The authors investigated the expressions of TNF-α,IL-1,IL-6 and IL-10 in the peripheral blood of heat stress rats and ulinastatin intervention in the early stage of heat stress.Methods Thirty SD rats were equally randomized into 3 groups: normal control,heat stress and ulinastatin intervention.Blood samples were collected from each group at 6,12 and 24 hours after construction of the rat models for determining the levels of TNF-α,IL-1,IL-6 and IL-10 by ELISA,and the body temperature,heart rate,systolic blood pressure and respiratory frequency were recorded at same time.Results The levels of TNF-α,IL-1,IL-6 and IL-10 were significantly higher in the heat stress group than in the normal controls at each time point(P0.01),but that of IL-10 decreased gradually.In the ulinastatin intervention group,the levels of TNF-α,IL-1 and IL-6 were remarkably lower(P0.01),that of IL-10 markedly higher(P0.01),and the body temperature,heart rate,systolic blood pressure and respiratory frequency significantly lower(P0.01) than in the heat stress group.Conclusion The proinflammatory factor secretion was remarkably increased with obvious systemic inflammatorome in the heat stress rats,but showed a downtrend 24 hours after heat stress.Early ulinastatin intervention could achieve a bilateral immune modulation by reducing the levels of TNF-α,IL-1 and IL-6 and increasing that of IL-10.
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