NLRP3炎症小体及其介导的细胞焦亡与急性心肌梗死后造影剂所致急性肾损伤的关系  

Relationship between NLRP3 Inflammasome and its Mediated Pyroptosis and Contrast-induced Acute Kidney Injury after Acute Myocardial Infarction

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作  者:提拉柯孜·图尔荪 魏海燕[1] 艾力·伊马木 杨和银[1] Tilakezi Tuersun;WEI Haiyan;Aili Yimamu(Department of Cardiology,The First People′s Hospital of Kashi,Xinjiang 844000,China)

机构地区:[1]喀什地区第一人民医院心内科,844000

出  处:《医学研究杂志》2024年第11期77-83,共7页Journal of Medical Research

基  金:新疆维吾尔自治区自然科学基金资助项目(2022D01F12)。

摘  要:目的 探讨NLRP3炎症小体及其介导的细胞焦亡与急性心肌梗死后造影剂所致急性肾损伤(contrast-induced acute kidney injury, CI-AKI)的关系。方法 构建急性心肌梗死后CI-AKI大鼠模型10只作为CI-AKI组,健康大鼠10只作为对照组。采用实时荧光定量聚合酶链反应(real-time fluorescence quantitative polymerase chain reaction, RT-qPCR)、Western blot法检测两组NLRP3炎症小体活化指标NLRP3、caspase-1mRNA及蛋白表达水平,以明确NLRP3与CI-AKI的关系。采用透射电镜观察两组肾脏组织形态变化,并采用酶联免疫吸附试验(enzyme-linked immunosorbent assay, ELISA)法检测两组细胞焦亡相关炎性指标白细胞介素-1β(interleukin-1β, IL-1β)、白细胞介素-18(interleukin-18, IL-18)水平,加以明确细胞焦亡与CI-AKI的关系。培养大鼠肾小管细胞,构建NLRP3过表达、沉默及空白对照组,明确NLRP3与细胞焦亡的关系。结果 RT-qPCR、Western blot法检测结果显示,CI-AKI组NLRP3mRNA及蛋白表达水平高于对照组(P<0.05)。透射电镜结果显示,CI-AKI组大鼠线粒体结构被破坏,线粒体空泡化,线粒体嵴明显减少,并且不清晰;另外,CI-AKI组细胞焦亡相关炎性指标IL-1β、IL-18水平较对照组高。大鼠肾小管NLRP3过表达、沉默及空白对照组间细胞焦亡相关炎性指标IL-1β、IL-18比较,差异均有统计学意义(P<0.05)。结论 在急性心肌梗死后CI-AKI中NLRP3表达水平升高,并诱导细胞焦亡;NLRP3水平越高,细胞焦亡越明显,提示NLRP3有望成为CI-AKI新的生物学标志物,为CI-AKI诊疗及预后评估提供新的参考依据。Objective To investigate the relationship between NLRP3 inflammasome and its mediated pyroptosis and contrast-induced acute kidney injury(CI-AKI)after acute myocardial infarction.Methods Ten CI-AKI rat models after acute myocardial infarction were constructed as the CI-AKI group,and 10healthy rats were used as the control group.Real-time fluorescence quantitative polymerase chain reaction(RT-qPCR)and Western blot were used to detect the mRNA and protein expression levels of NLRP3 inflammasome activation markers NLRP3 and caspase-1 in the two groups to clarify the relationship between NLRP3 and CI-AKI.The morphological changes of renal tissue in the two groups were observed by transmission electron microscopy,and the levels of interleukin-1β(IL-1β)and interleukin-18(IL-18)were detected by enzyme-linked immunosorbent assay(ELISA)to clarify the relationship between pyroptosis and CI-AKI.Rat renal tubular cells were cultured to construct NLRP3 overexpression,silencing and blank control groups to clarify the relationship between NLRP3 and pyroptosis.Results The results of RT-qPCR and Western blot showed that the expression of NLRP3mRNA and protein in CI-AKI group was higher than that in control group(P<0.05).Transmission electron microscopy can clearly see that the mitochondrial structure of the CI-AKI group was destroyed,the mitochondria were vacuolated,and the mitochondrial cristae were significantly reduced and unclear;in addition,the levels of pyroptosis-related inflammatory indicators IL-1βand IL-18 in the CI-AKI group were higher than those in the control group.There were significant differences in pyroptosis-related inflammatory indicators IL-1βand IL-18 between rat renal tubular NLRP3 overexpression,silencing and blank control groups(P<0.05).Conclusion The expression level of NLRP3 increased in CI-AKI after acute myocardial infarction,which induced pyroptosis;the higher the level of NLRP3,the more significant the cell pyroptosis.NLRP3 is expected to become a new biological marker of CI-AKI,providing a new

关 键 词:NLRP3炎症小体 细胞焦亡 造影剂所致急性肾损伤 

分 类 号:R541.4[医药卫生—心血管疾病]

 

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