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作 者:徐家行 陈宝钧[1] 刘勇 张亚楠 殷桂林 XU Jiahang;CHEN Baojun;LIU Yong;ZHANG Yanan;YIN Guilin(Department of Thoracic Surgery,the Central Hospital of Wuhan,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430014,China)
机构地区:[1]华中科技大学同济医学院附属武汉中心医院胸外科,武汉430014 [2]中国人民解放军中部战区总医院心胸外科,武汉430070
出 处:《实用医学杂志》2019年第24期3736-3740,共5页The Journal of Practical Medicine
基 金:全军“十二五”医学科研资助项目(编号:CWS11J019);湖北省自然科学基金项目(编号:2018CFB793)
摘 要:目的研究核转录因子-κB(nuclear factor-κB,NF-κB)通路在BQ-123与单肺通气预处理干预兔单肺通气肺损伤的作用。方法大耳白兔15只随机分为3组。O组为兔单肺通气实验的模型组;OP组在单肺通气处理前注射BQ-123进行处理;BP组在单肺通气前予以单肺通气预处理联合注射BQ-123处理。实验结束后留取左下肺组织检测内皮素-1(endothelin-1,ET-1)、肺组织中炎症相关因子[肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)]、凋亡相关因子[半胱氨酸天冬氨酸蛋白酶-3(caspase-3)];计算细胞凋亡指数(apoptotic index,AI);测定各组单肺通气肺组织中NF-κB通路的关键因子NF-κBp65及IκBα蛋白表达检测。结果O组、OP组和BP组相比较,ET-1、TNF-α、caspase-3、AI及NF-κB p65蛋白3组依次升高,3组之间差异有统计学意义(P<0.05);IκBα蛋白3组间依次上升,3组之间差异有统计学意义(P<0.05)。结论NF-κB通路可以减轻对兔单肺通气肺损伤程度。Objective To investigate the possible effects of NF-κB(nuclear factor-κB)signaling pathway on lung injury with BQ-123 and one-lung ventilation preconditioning in rabbits.Methods 15 rabbits were randomly divided into three groups.In Group O,the rabbits treated with single lung ventilation and served as experiment models.In Group OP,the models were pre-injected with BQ-123.In Group BP,the models were treated with single lung ventilation pretreatment combined with BQ-123.After experiments,the left lower lung tissues were collected and the expressions of endothelin-1(ET-1),inflammation-related factors,tumor necrosis factor-α(TNF-α),apoptosis-related factor caspase-3,the apoptotic index(AI)was detected.And the expressions of NF-κBp65 and IκBαprotein in lung tissue of each group was determined.Results ET-1,TNF-α,caspase-3,AI and NF-κBp65 proteins were increased in all three groups.There were significant differences between the three groups(P<0.05);IκBαprotein in the three groups increased gradually and there were statistically significant differences between three groups(P<0.05).Conclusion NF-κB signaling pathway may play a suppressive role in the regulation of lung injury in rabbits.
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