Effects of salidroside regulates UCHL1 expression and inhibits the apoptosis of keloid fibroblasts
Objective To investigate the mechanism of salidroside on abnormal proliferation and extracellular matrix deposition of keloid(KD)fibroblasts.Methods The primary KD fibroblasts were randomly divided into model group(normal culture),experimental-L group(50 μmol·L-1 salidroside),experimental-H group(100 μmol·L-1 salidroside),Vector group(100 μmol·L-1 salidroside+Vector),ubiquitin C-terminal hydrolase L1(UCHL1)group(100 μmol·L-1 salidroside+overexpression UCHL1);The mRNA expression level of UCHL1 was detected by real-time fluorescence quantitative polymerase chain reaction(RT-qPCR);flow cytometry was used to detect apoptosis;Western blot assay was used to detect the expression levels of Collagen Ⅰ,glutathione peroxidase 4(GPX4)and α-smooth muscle actin(α-SMA);the reactive oxygen species(ROS)levels was detected by DCFH-DA method.Results The relative expression levels of UCHL1 mRNA in model group,experimental-L,experimental-H,vector group and UCHL1 group were 1.01±0.11,0.71±0.07,0.49±0.05,0.50±0.05 and 2.36±0.13,respectively;the apoptosis rates were(4.59±0.56)％,(12.11±0.80)％,(22.16±3.21)％,(23.54±2.08)％,(9.04±0.72)％,respectively;Collagen Ⅰ protein expression levels were 0.97±0.06,0.82±0.07,0.53±0.04,0.54±0.07 and 0.91±0.11,respectively;α-SMA protein expression levels were 1.11±0.07,0.79±0.06,0.61±0.08,0.60±0.04,0.96±0.11,respectively;GPX4 protein expression levels were 0.93±0.06,0.66±0.04,0.41±0.03,0.43±0.03,0.78±0.04,respectively;ROS levels were(100.00±5.03)％,(127.18±10.15)％,(146.09±10.15)％,(144.75±10.95)％,(106.57±11.28)％,respectively.Compared with the model group,the above indexes in the experimental-L,-H groups were statistically significant(all P＜0.05).Compared with the Vector group,the above indexes in the UCHL1 group were statistically significant(all P＜0.05).Conclusion Salidroside can induce iron death,promote fibroblast apoptosis,inhibit excessive extracellular matrix deposition,and slow down KD progression,which may be related to the inhibition of UCHL1 expression.
万方数据
维普
