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作 者:邹宪宝[1] 李新宇[2] 任屹[2] 张雷[2] 周新[2] 王晓燕[2] 信文启[1] 陈姚[1] 杨晴[1]
机构地区:[1]新疆石河子大学医学院,石河子832002 [2]兰州军区乌鲁木齐总医院
出 处:《内科急危重症杂志》2011年第3期160-162,共3页Journal of Critical Care In Internal Medicine
摘 要:目的:观察严重脓毒症患者血清对人肺血管内皮细胞(pulmonary microvascular endothelial cell,PMVECs)NF-kB表达的影响,探讨严重脓毒症致急性肺损伤的发生机制。方法:随机将离体培养PMVECs分为3组:正常培养组(加入10%胎牛血清,A组)、健康血清组(加入10%健康人血清,B组)、患者血清组(加入10%严重脓毒症患者血清,C组),分别于刺激0、1、2、4、6h免疫组化观察离体PMVECs NF-κB表达并测定各组平均光密度(average optical density,AOD)值;ELISA法检测培养上清液分泌的TNF-α水平;比较不同时相3组PMVECs上述指标变化。结果:与A组及B组相比,C组PMVECs胞核NF-κB呈强阳性表达,且1h AOD值达高峰,后逐渐下降(0.523±0.012,0.498±0.009,0.444±0.030);ELISA显示:不同时相A组与B组TNF-α水平均无明显差异(P>0.05),C组与A组、B组相比各时间点TNF-α水平均明显升高,且均有显著差异(P<0.01)。结论:严重脓毒症患者血清可通过活化NF-κB启动分泌TNF-α,这可能是严重脓毒症致急性肺损伤的一个重要通路。Objective:To observe the effect of serum of sepsis patients on the expression of Nuclear Factor-Kappa B(NF-κB) on human pulmonary vascular endothelial cells(PMVECs),and to explore the mechanism of severe sepsis induced acute lung injury(ALI).Methods:PMVECs were cultured in vitro,and were divided into 3 groups randomly:normal culture group(group A),healthy serum group(group B),patients' serum group(group C).The expressions of NF-κB were obseverd and values of average optical density(AOD) were detected by immunohistochemistry at 0,1h,2h,4h,6h after stimulation.Concentration of TNF-α was detected by ELISA.The above indexes of pulmonary vascular endothelial cells were compared between 3 groups.Results:Compared with that of group A and group B,the expression of NF-κB in PMVECs showed strongly positive in group C,and AOD values reached peak at 1 hour,and decreased gradually(0.523±0.012,0.498±0.009,0.444±0.030).No significant difference of TNF-α between group A and group B was found(P0.05).Compared with that of group A and group B,the level of TNF-α was significantly increased at each time point,and showed significant differences(P0.01).Conclusion:Serum of severe sepsis patients can activate NF-κB and thus initiate the secretion of TNF-α,which may be an important pathway of ALI caused by severe sepsis.
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