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血管紧张素Ⅱ对H9C2细胞中NLRP3炎性体的作用
李卫东,李奕霖,罗勇,陈丽,吕湛
0
(川北医学院附属医院心内科;川北医学院第二附属医院心内科)
摘要:
【摘要】 目的 探讨血管紧张素Ⅱ(AngⅡ)对H9C2细胞中NLRP3的作用。方法 培养H9C2细胞株,选用对数生长期的H9C2细胞进行试验,用106mol/l的AngⅡ予以刺激,于不同的时间点收集细胞,通过实时荧光定量PCR(RTqPCR)及蛋白质印迹法(Western blot)分别检测细胞中NLRP3、ASC、Caspase1、IL1β的基因和蛋白水平;通过酶联免疫吸附法(ELISA)检测细胞培养液上清液中IL1β的含量。结果 NLRP3、ASC、Caspase1及IL1β的基因相对表达量在各处理组与0h组相比差异有统计学意义(P<005)。Caspase1及IL1β的蛋白相对表达量在各处理组与0h组相比差异有统计学意义(P<005)。细胞培养液上清液中IL1β的含量在各处理组与0h组相比差异有统计学意义(P<005)。结论 血管紧张素Ⅱ可促使H9C2细胞中NLRP3、ASC、Caspase1和IL1β的基因及蛋白表达水平增加,同时也可使细胞培养液上清液中IL1β的含量增加;AngⅡ可通过激活NLRP3炎性小体导致心肌细胞慢性炎症的发生而导致心肌重构,参与心肌病的发生发展过程。
关键词:  血管紧张素Ⅱ  H9C2细胞株  NLRP3炎性体  IL 1β  心肌重构
DOI:
基金项目:四川省教育厅科研项目(16ZB0228)
Department of Cardiology, The Affiliated Hospital of North Sichuan Medical College
LI Weidong,LI Yilin,LUO Yong,CHEN Li,LV Zhan
(Department of Cardiology, The Affiliated Hospital of North Sichuan Medical College;Department of Cardiology, The Second Affiliated Hospital of North Sichuan Medical College)
Abstract:
【Abstract】 Objective To explore the effects of angiotensinII on NLRP3 inflammation in H9C2 cells.Methods All experiments were performed by using of the H9C2 cells, which were cultured in vitro and treated with 106mol/l of AngⅡ. The cells were collected at varying time point.Expression levels of NLRP3, ASC, Caspase1, IL1β mRNA were detected with quantitative realtime PCR, expression levels of NLRP3, ASC, Caspase1, IL1β protein were detected by western blot, and the content of inflammatory factors in supernatant detected through ELISA.Results The expression of mRNA levels of NLRP3, ASC, Caspase1 and IL1β were significantly higher than that with 0h group (P<005). The expression of protein levels of NLRP3, ASC, Caspase1 and IL1β were significantly higher than those in 0h group(P<005). The content of inflammatory factors IL1β in the supernatant were significantly higher than those in the 0h group (P<005).Conclusion Treatment on H9C2 cells with AngⅡ could give rise to the mRNA and protein expression levels of NLRP3, ASC, Caspase1 and IL1β,and increase the content of IL1β in the supernatant. AngiotensinII could induce inflammation of cardiomyocytes by activating NLRP3 inflammatory bodies, and this process is associated with angiotensinII leading to cardiomyopathy.
Key words:  AngⅡ  H9C2  NLRP3  IL 1β

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