吴明月,黄紫霞,许锋,龚俊,熊韬,王睎之,王德明.扁塑藤素对LPS诱导的HUVEC细胞功能损伤和焦亡的作用.[J].中南医学科学杂志.,2022,(2):175-178.
扁塑藤素对LPS诱导的HUVEC细胞功能损伤和焦亡的作用
Effects of pristimerin on dysfunction and pyroptosis of HUVEC induced by LPS
投稿时间:2021-07-13  修订日期:2021-12-10
DOI:10.15972/j.cnki.43-1509/r.2022.02.005
中文关键词:  扁塑藤素  人脐静脉内皮细胞  脂多糖  焦亡
英文关键词:pristimerin  HUVEC  lipopolysaccharide  pyroptosis
基金项目:湖南省卫计委资助项目(B2016134) 作者简介:吴明月,硕士研究生,研究方向为围术期器官功能保护,E-mail为wumingyue111@163.com。通信作者王德明,博士,主任医师,硕士研究生导师,研究方向为围术期器官功能保护,E-mail为wdm1998@163.com。
作者单位E-mail
吴明月 南华大学衡阳医学院附属第二医院麻醉科,湖南省衡阳市421001 e-mail为wumingyue111@163.com,e-mail为wdm1998@163.com 
黄紫霞 南华大学衡阳医学院附属第二医院麻醉科,湖南省衡阳市421001  
许锋 南华大学衡阳医学院附属第二医院麻醉科,湖南省衡阳市421001  
龚俊 南华大学衡阳医学院附属第二医院麻醉科,湖南省衡阳市421001  
熊韬 南华大学衡阳医学院附属第二医院麻醉科,湖南省衡阳市421001  
王睎之 南华大学船山学院,湖南省衡阳市421001  
王德明 南华大学衡阳医学院附属第二医院麻醉科,湖南省衡阳市421001 e-mail为wumingyue111@163.com,e-mail为wdm1998@163.com 
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中文摘要:
      目的研究扁塑藤素对脂多糖(LPS)诱导人脐静脉血管内皮细胞(HUVEC)损伤的保护作用及可能机制。方法 建立LPS诱导HUVEC损伤模型,HUVEC细胞分为对照组、LPS组以及低、中、高剂量扁塑藤素组(0.1、0.2、0.4 μmol/L扁塑藤素)。CCK-8法测定细胞活力;试剂盒法检测乳酸脱氢酶(LDH)、丙二醛(MDA)、超氧化物歧化酶(SOD)含量;ELISA法检测白细胞介素-1β(IL-1β)、IL-18蛋白水平;蛋白免疫印迹法、实时荧光定量PCR法检测焦亡相关分子NLRP3、Caspase-1、GSDMD蛋白和mRNA表达量。 结果与对照组比较,LPS组细胞活力和SOD含量显著下降(P<0.05),LDH和MDA含量、NLRP3、Caspase-1、GSDMD的蛋白和mRNA表达量均显著升高(P<0.05)。扁塑藤素呈剂量依赖性提高细胞活力和SOD含量,抑制LDH、MDA,降低NLRP3、Caspase-1、GSDMD的蛋白和mRNA表达水平(P<0.05)。 结论扁塑藤素呈剂量依赖性抑制细胞焦亡和减轻氧化应激,从而改善LPS诱导的HUVEC功能损伤。
英文摘要:
      To study the protective effect and possible mechanism of Pristimerin (Pri) on damage of human umbilical vein endothelial cell (HUVEC) induced by lipopolysaccharide (LPS). Methods A model of HUVEC injury induced by LPS was established. The cell were divided into control group, LPS group, and low, medium, high dose pristimerin group (0.1,0.2 and 0.4 μmol/L). Cell viability was determined by CCK-8 method. The lactate dehydrogenase (LDH), malondialdehyde (MDA) and superoxide dismutase (SOD) were detected by kit method, and interleukin-1β(IL-1 β), IL-18 protein level was detected by ELISA. The protein and mRNA expressions of NLRP3, Caspase-1 and GSDMD were detected by Western blotting and qRT-PCR. ResultsCompared with the control group, the cell viability and SOD content in LPS group decreased significantly (P<0.05), and LDH and MDA, NLRP3, Caspase-1 and GSDMD protein and mRNA increased significantly (P<0.05). Pristimerin increased cell viability and SOD, inhibited LDH and MDA, and decreased the protein and mRNA expression of NLRP3, Caspase-1 and GSDMD in a dose-dependent manner (P<0.05). ConclusionPristimerin can improve the LPS induced dysfunction of HUVEC by inhibiting cell pyroptosis and reducing oxidative stress in a dose-dependent manner.
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