| 注册
首页|期刊导航|中国免疫学杂志|IL-37通过调控NF-κB通路抑制人主动脉血管平滑肌细胞成骨转化并参与抑制其钙化

IL-37通过调控NF-κB通路抑制人主动脉血管平滑肌细胞成骨转化并参与抑制其钙化

马晨越 贺琼逸 王猛 柴萌 张海涛

中国免疫学杂志2025,Vol.41Issue(2):304-309,6.
中国免疫学杂志2025,Vol.41Issue(2):304-309,6.DOI:10.3969/j.issn.1000-484X.2025.02.008

IL-37通过调控NF-κB通路抑制人主动脉血管平滑肌细胞成骨转化并参与抑制其钙化

IL-37 inhibits osteogenic transformation of human aortic vascular smooth muscle cells and participates in inhibition of their calcification via TLR/NF-κB pathway

马晨越 1贺琼逸 1王猛 2柴萌 3张海涛1

作者信息

  • 1. 安徽医科大学空军临床学院,安徽医科大学第五临床学院,合肥 230032||空军特色医学中心心内科,北京 100142
  • 2. 河北北方学院,张家口 075000
  • 3. 首都医科大学附属北京安贞医院心内科,北京市心肺血管病研究所,北京市冠状动脉粥样硬化疾病精准医学重点实验室,首都医科大学冠心病临床中心,北京 100029
  • 折叠

摘要

Abstract

Objective:To investigate the effect of IL-37 on oxidized low-density lipoprotein(ox-LDL)-induced calcification in human aortic vascular smooth muscle cells(HA-SMCs)and the influence of toll-like receptor(TLR)/nuclear transcription factor(NF-κB)pathway and osteogenic transcription factors,to demonstrate the mechanism of IL-37 in calcification.Methods:The calcifica-tion model of HA-SMCs was treated with ox-LDL,and the model group was pretreated with 100 ng/ml IL-37 or 100 µmol/L PDTC.CCK8 was used to detect cell proliferation activity;flow cytometry was used to detect apoptosis.Alizarin red staining was used to detect calcified nodules.The mRNA levels of smooth muscle actin(SMA),bone morphogenetic protein(BMP2)and IL-37 were detected by qPCR;mRNA and protein expression levels of TLR,NF-κB,p-NF-κB,RUNX-associated transcription factor(RUNX2),alkaline phosphatase(ALP),SMA and smooth muscle 22α(SM22α)were detected by qPCR and Western blot.Results:Compared with the control group,ox-LDL treatment enhanced cellular proliferation activity and was concentration-dependent(P<0.05),and apoptosis rate was increased,while the model group produced significant orange-red calcified nodules,up-regulated mRNA and protein expres-sion of inflammatory factors such as TLR and NF-κB,up-regulated mRNA expression of IL-37,RUNX2,BMP2,ALP,while SMA and SM22α mRNA expressions were decreased,and the protein expressions of p-NF-κB and RUNX2 were increased significantly;compared with the modeling group,the IL-37 pretreatment group showed lower viability and decreased apoptosis rate(P<0.05),sig-nificantly reduced calcified nodules,and the mRNA and protein expression of inflammatory factors such as TLR and NF-κB,and mRNA of RUNX2,BMP2,ALP expressions were downregulated,mRNA expression of SMA and SM22α were elevated,and protein expressions of p-NF-κB and RUNX2 were significantly decreased,showing the same trend as the inhibitor PDTC group in cytokines.Conclusion:IL-37 inhibits calcification of HA-SMCs,which may be related to the inhibition of NF-κB pathway and osteogenic pheno-type transformation.

关键词

IL-37/人主动脉血管平滑肌细胞/成骨转化/TLR/NF-κB通路

Key words

IL-37/Human aortic vascular smooth muscle cells/Osteogenic transformation/TLR/NF-κB pathway

分类

基础医学

引用本文复制引用

马晨越,贺琼逸,王猛,柴萌,张海涛..IL-37通过调控NF-κB通路抑制人主动脉血管平滑肌细胞成骨转化并参与抑制其钙化[J].中国免疫学杂志,2025,41(2):304-309,6.

基金项目

军队医学科技青年培育计划拔尖项目(20QNPY062) (20QNPY062)

北京医院管理局孵化项目(PX2022023). (PX2022023)

中国免疫学杂志

OA北大核心

1000-484X

访问量0
|
下载量0
段落导航相关论文