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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
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摘要 目的探讨冬凌草甲素(ORI)对人瘢痕疙瘩来源的成纤维细胞(HKF)的影响及作用机制。方法CCK-8法检测ORI对HKF的增殖活性的影响,实验分为对照组和实验组,细胞划痕和transwell实验检测HKF的迁移和侵袭能力,实时荧光定量PCR(RT-qPCR)和蛋白免疫印迹法(Western blot)检测ORI对HKF的细胞外基质形成相关mRNA和纤维连接蛋白1(FN1)、α-平滑肌肌动蛋白(α-SMA)、Ⅰ型胶原蛋白(COLⅠ)、COLⅢ表达的影响。实验分为对照组、模型组和转化生长因子(TGF)-β1+ORI组,用RT-qPCR和Western blot检测ORI对HKF内TGF-β1诱导的相关mRNA和核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)、凋亡相关斑点样蛋白(ASC)、Smad2、Smad3、磷酸化Smad2蛋白(p-Smad2)、p-Smad3表达的影响。结果CCK-8显示随着ORI浓度增加,HKF细胞抑制率逐渐增加;与对照组比较,实验组细胞24 h迁移面积、侵袭细胞数显著下降,FN1、α-SMA、COL I、COLⅢ表达水平显著下降(P<0.05);与对照组相比,模型组NLRP3、ASC、Smad2、Smad3、p-Smad2、p-Smad3表达显著升高(P<0.05);与模型组相比,TGF-β1+ORI组NLRP3、ASC、Smad2、Smad3、p-Smad2、p-Smad3表达显著下降(P<0.05)。结论ORI通过阻断TGF-β1/Smad信号通路和NLRP3介导的炎症反应,抑制HKF的增殖、迁移和侵袭能力以及细胞外基质的形成和沉积。 Objective To investigate the effects and mechanisms of oridonin(ORI)on human keloid-derived fibroblasts(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 fibronectin 1(FN1),α-smooth muscle actin(α-SMA),type I collagen(COL I),and COLⅢin HKF.The experiment 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 nucleotide-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 concentrations of ORI.Compared with the control group,the experimental group exhibited a significant reduction in the migration area at 24 hours and a decrease in the number of invasive cells.Furthermore,there was a significant downregulation in the expression levels of FN1,α-SMA,COL I,and COLⅢ(P<0.05).In comparison with the control 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 significant 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 inflammatory response.
作者 宋采滢 高翔 朱秋璇 程盛荣 陈文东 朱飞 Song Caiying;Gao Xiang;Zhu Qiuxuan;Cheng Shengrong;Chen Wendong;Zhu Fei(Dept of Plastic Surgery,The First Affiliated Hospital of Anhui Medical University,Hefei 230022)
出处 《安徽医科大学学报》 CAS 北大核心 2024年第10期1706-1712,共7页 Acta Universitatis Medicinalis Anhui
基金 国家自然科学基金项目(编号:30973124) 安徽高校省级自然科学研究项目(编号:KJ2014A108)。
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 oridonin human keloid fibroblasts extracellular matrix NLRP3 TGF-β1 Smad proteins
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