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作 者:张培 朱新旺[1] 孙亚南[1] 穆中一[2] ZHANG Pei;ZHU Xinwang;Sun Yanan;MU Zhongyi(Department of Nephrology,First Affiliated Hospital of China Medical University,Shenyang,Liaoning 110000,China;Department of Urological Surgery,Liaoning Provincial Tumor Hospital,Shenyang,Liaoning 110000,China)
机构地区:[1]中国医科大学附属第一医院肾内科,沈阳110000 [2]辽宁省肿瘤医院泌尿外科,沈阳110000
出 处:《重庆医学》2022年第9期1458-1462,共5页Chongqing medicine
基 金:辽宁省自然科学基金项目(20170540560)。
摘 要:目的探讨血液透析对肾衰大鼠心功能的影响及机制。方法将40只大鼠分为假手术组、模型组、激动剂组和血液透析组,除假手术组外,其余组建立肾衰模型。结果模型组大鼠心肌细胞肥大,细胞核溶解,心肌纤维排列紊乱,大量炎症细胞浸润;激动剂组和血液透析组大鼠心肌组织病理损伤减轻;与模型组比较,血液透析组左心室舒张末压(LVEDP)升高,左心室收缩压(LVSP)、左心室内压最大上升速率(+dp/dtmax)、左心室内压最大下降速率(-dp/dtmax)、血肌酐、尿素氮、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、IL-1β水平及Toll样受体4(TLR4)、caspase-3 mRNA水平和蛋白水平,以及p-NF-κB p65蛋白水平、p-NF-κB p65/NF-κB p65降低(P<0.05);与血液透析组比较,激动剂组LVEDP降低,其余各指标升高(P<0.05)。结论血液透析可减轻肾衰大鼠肾损伤及心肌炎症,改善心功能,可能是通过抑制TLR4/NF-κB信号通路发挥作用。Objective To investigate the effect and mechanism of hemodialysis on the heart function in the rats with renal failure.Methods Forty rats were divided into the sham operation group,model group,agonist group and hemodialysis group,except for the sham operation group,the other groups were established the renal failure model.Results In model group,there were the myocardial cell hypertrophy,nucleolysis,myocardial fiber arrangement disorder and a large number of inflammatory cells infiltration;the pathological damage of myocardial tissue in the agonist group and hemodialysis group was reduced.Compared with the model group,LVEDP,LVSP,+dp/dtmax,-dp/dtmax,serum creatinine,urea nitrogen,CK,CK-MB,IL-6,TNF-α,IL-1β,TLR4,caspase-3 mRNA and protein levels in the hemodialysis group were increased,and the protein level of p-NF-κB p65,p-NF-κB p65/NF-κB p65 were decreased(P<0.05).Compared with the hemodialysis group,LVEDP in the agonist group was decreased,and the other indexes were increased(P<0.05).Conclusion Hemodialysis can reduce the renal injury and myocardial inflammation and improve the cardiac function in the rats with renal failure,which plays the role possibly by inhibiting TLR4/NF-κB signaling pathway.
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