安徽医科大学学报2024，Vol.59Issue(10)：1706-1712,7.DOI:10.19405/j.cnki.issn1000-1492.2024.10.003
冬凌草甲素对人瘢痕疙瘩来源的成纤维细胞生物学行为的影响及作用机制
Effect and mechanism of oridonin on malignant biological behavior of keloid fibroblasts
摘要
Abstract
Objective To investigate the effects and mechanisms of oridonin(ORI)on human keloid-derived fi-broblasts(HKF).Methods The effects of ORI on the proliferation activity of HKF were assessed using the CCK-8 assay.The experiment was divided into control and experimental groups.Cell scratch and Transwell assays were conducted to evaluate the migration and invasion capabilities of HKF.Real-time quantitative PCR(RT-qPCR)and Western blot were used to examine the impact of ORI on the expression of extracellular matrix-related mRNA and fi-bronectin 1(FN1),α-smooth muscle actin(α-SMA),type Ⅰ collagen(COL Ⅰ),and COL Ⅲ in HKF.The ex-periment was also divided into control,model,and transforming growth factor(TGF)-β1+ORI groups.RT-qPCR and Western blot were utilized to determine the effects of ORI on the expression of TGF-β1-induced mRNA and nu-cleotide-binding oligomerization domain-like receptor protein 3(NLRP3),apoptosis-associated speck-like protein containing a CARD(ASC),Smad2,Smad3,phosphorylated Smad2(p-Smad2),and p-Smad3 in HKF.Results CCK-8 assay demonstrated that the cell inhibition rate of HKF progressively increased with increasing concentra-tions of ORI.Compared with the control group,the experimental group exhibited a significant reduction in the mi-gration area at 24 hours and a decrease in the number of invasive cells.Furthermore,there was a significant down-regulation in the expression levels of FN1,α-SMA,COL Ⅰ,and COL Ⅲ(P＜0.05).In comparison with the con-trol group,the model group showed a significant upregulation in the expression of NLRP3,ASC,Smad2,Smad3,p-Smad2,and p-Smad3(P＜0.05).Relative to the model group,the TGF-β1+ORI group demonstrated a signifi-cant downregulation in the expression of NLRP3,ASC,Smad2,Smad3,p-Smad2,and p-Smad3(P＜0.05).Conclusion ORI the proliferation,migration,and invasiveness of HKF,as well as the formation and deposition of the extracellular matrix,through the blockade of the TGF-β1/Smad signaling pathway and the NLRP3-mediated in-flammatory response.关键词
冬凌草甲素/人瘢痕疙瘩来源的成纤维细胞/细胞外基质/NLRP3/TGF-β1/Smad蛋白Key words
oridonin/human keloid fibroblasts/extracellular matrix/NLRP3/TGF-β1/Smad proteins分类
医药卫生引用本文复制引用
宋采滢,高翔,朱秋璇,程盛荣,陈文东,朱飞..冬凌草甲素对人瘢痕疙瘩来源的成纤维细胞生物学行为的影响及作用机制[J].安徽医科大学学报,2024,59(10):1706-1712,7.基金项目
国家自然科学基金项目(编号:30973124) （编号:30973124）
安徽高校省级自然科学研究项目(编号:KJ2014A108) National Natural Science Foundation of China(No.30973124) （编号:KJ2014A108）
Natural Science Research Pro-ject in Higher Education Institutions of Anhui Province(No.KJ2014A108) （No.KJ2014A108）
