人参皂苷Rh2调控微小RNA-133a-3p对瘢痕疙瘩成纤维细胞凋亡的影响  

Effect of ginsenoside Rh2 on the apoptosis of keloid fibroblasts by regulating miR-133a-3p

作　　者：周自广[1] ZHOU Ziguang(Department of Dermatology,The First People's Hospital of Zhengzhou,Zhengzhou,Henan 450000,China)

机构地区：[1]郑州市第一人民医院皮肤科,河南郑州450000

出　　处：《安徽医药》2022年第5期873-876,共4页Anhui Medical and Pharmaceutical Journal

摘　　要：目的探讨人参皂苷Rh2调控微小RNA(miR)-133a-3p对瘢痕疙瘩成纤维细胞(KF)凋亡的影响。方法用浓度为50、100、200 mg/L的人参皂苷Rh2培养KF,未给人参皂苷Rh2的KF记为对照(NC)组;将miR-NC、miR-133a-3p分别转染至KF中记为miR-NC组、miR-133a-3p组;将anti-miR-NC、anti-miR-133a-3p分别转染至KF再用200 mg/L的人参皂苷Rh2处理记为anti-miR-NC+人参皂苷Rh2组、anti-miR-133a-3p+人参皂苷Rh2组。流式细胞术检测细胞凋亡;实时荧光定量PCR(RT-qPCR)检测miR-133a-3p表达水平;蛋白质印迹法检测裂解的半胱氨酸天冬氨酸蛋白酶-3(Cleavedcaspase-3)、β-连环素(β-catenin)表达。结果与对照组相比,50、100、200 mg/L人参皂苷Rh2处理的KF中细胞凋亡率升高[(9.08±0.91)%、(16.28±1.63)%、(23.18±2.32)%比(4.29±0.43)%],miR-133a-3p表达水平升高,β-catenin表达水平降低(P<0.05)。过表达miR-133a-3p,Cleaved caspase-3表达水平升高,细胞凋亡率升高(P<0.05)。低表达miR-133a-3p部分逆转了人参皂苷Rh2对KF凋亡和β-catenin的影响。结论人参皂苷Rh2可促进瘢痕疙瘩成纤维细胞凋亡,其机制可能与miR-133a-3p和Wnt/β-catenin信号通路有关。Objective To investigate the effect of ginsenoside Rh2 on the apoptosis of keloid fibroblasts(KF)by regulating miR-133a-3p.Methods KF was cultured with ginsenoside Rh2 at different concentrations of 50,100,200 mg/L,and KF without ginsen⁃oside Rh2 was recorded as control(NC)group;miR-NC and miR-133a-3p were transfected to KF,which was recorded as miR-NC group and miR-133a-3p group;anti-miR-NC and anti-miR-133a-3p were transfected into KF and treated with 200 mg/L ginsenoside Rh2 as anti-miR-NC+ginsenoside Rh2 group,anti-miR-133a-3p+ginsenoside Rh2 group.Apoptosis was detected by flow cytometry;the expression of miR-133a-3p was detected by real-time quantitative PCR(RT-qPCR);the expression of cleaved cysteine-containing aspartate-specific proteases-3(Cleaved caspase-3)andβ-catenin was detected by Western blot.Results Compared with control group,the apoptosis rate of KF treated with 50,100,200 mg/L of ginsenoside Rh2 was significantly increased[(9.08±0.91)%,(16.28±1.63)%,(23.18±2.32)%vs.(4.29±0.43)%],the expression of miR-133a-3p was significantly increased,and the expression ofβ-catenin was sig⁃nificantly decreased(P<0.05).Overexpression of miR-133a-3p,the expression of Cleaved caspase-3 was significantly increased,and the apoptosis rate was significantly increased(P<0.05).Low expression of miR-133a-3p partially reversed the effect of ginsenoside Rh2 on KF apoptosis andβ-catenin.Conclusion Ginsenoside Rh2 promotes apoptosis of keloid fibroblasts,and its mechanism may be re⁃lated to miR-133a-3p and Wnt/β-catenin signaling pathways.

关 键 词：人参皂苷类 瘢痕疙瘩 成纤维细胞 微小RNA-133a-3p Wnt/β-连环素信号通路 凋亡 

分 类 号：R285[医药卫生—中药学]