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作 者:孟瑚[1] 周晓萍[1] 徐剑[1] 罗惠民[1] 熊丽焱[1]
机构地区:[1]云南省第一人民医院肾内科,云南昆明650032
出 处:《昆明理工大学学报(自然科学版)》2015年第2期108-113,共6页Journal of Kunming University of Science and Technology(Natural Science)
基 金:云南省科技厅应用基础研究基金项目(2011FZ275)
摘 要:研究亲环素A(Cy PA)在正常人群及急性肾损伤(AKI)患者外周血中的浓度变化,探讨Cy PA是否与急性肾损伤有关及其可能的作用机制.检测急性肾损伤患者外周血中厄贝沙坦治疗前后Cy PA、Ang II、TNFα、IL-6、IL-1α、MCP-1水平,并以正常人为对照组.结果发现AKI组外周血Cy PA水平治疗前高于正常对照组.AKI组Cy PA与Ang II及TNFα、IL-6、IL-1α正相关,与MCP-1负相关,相关系数分别为0.6,0.539,0.688,0.693,-0.725.说明Cy PA作为一种炎症细胞介质,可能协同Ang II,参与了AKI患者炎性反应,加重肾小管上皮细胞损伤及细胞凋亡.通过选择性地抑制或阻断Cy PA或Ang II受体可能为我们提供一条对急性肾损伤的新治疗途径.CyPA concentration levels in the peripheral blood in the normal subjects and patients with acute kid-ney injury (AKI)are detected to determine whether CyPA is associated with acute kidney injury and its possible mechanism.The level of CyPA,AngII,TNFα,IL -6,IL -1 and MCP -1 are measured in patients with AKI before and after treatment with irbesatan for 4 weeks.The positive control group is composed of normal subjects.It is observed that the level of CyPA in peripheral blood of AKI group is higher than that in the normal control group,The correlation coefficient of CyPA and AngII,IL -6,IL -1,TNF and MCP -1 are 0.6,0.539,0.688, 0.693,-0.725 respectively .The results show that CyPA may act as an inflammatory cell medium which coop-erates with AngII ,promotes AKI patients with inflammatory reaction,and increases renal tubular and interstitial injury.CyPA may be a new marker of inflammation in AKI damage.Through selective inhibition of CyPA or blocking of AngII receptors may provide a new treatment of AKI.
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