重庆医学2017，Vol.46Issue(5)：580-582,585,4.DOI:10.3969/j.issn.1671-8348.2017.05.002
A型肉毒毒素对增生性瘢痕成纤维细胞的抑制作用及机制
Study of mechanism and inhibition of botulinum toxin type A on hypertrohic scar fibroblasts
摘要
Abstract
Objective To explore the mechanism and inhibition of botulinum toxin type A (BTXA) on hypertrohic scar fibroblasts.Methods The cells were treated by 0 (control),0.2,0.4,0.8 U/ml BTXA for 48 h.Cell viability was detected by MTT assay.Cell apoptosis was detected by Hoechst staining.Cell cycle was detected by flow cytometry.The level of cell cycle related protein D1 (Cyclin D1),proliferation nuclear antigen (PCNA) and activation of phosphatidylinositol 3 kinase (PI3K) / protein kinase B (AKT) signaling pathway were assayed by western blot.Results Compared with control group(0.75±0.07),0.2,0.4,0.8 U/mL BTXA(0.59 ± 0.06,0.43 ± 0.04,0.34± 0.03) inhibited hypertrohic scar fibroblasts cell viability,increased cell apoptotic rate[control group(2.38±0.24)％;BTXA(15.79±1.54)％,(27.32±2.69)％,(38.46±3.90)％],down-regulated the expression of Cyclin D1(control group 1.57±0.18;BTXA 0.93±0.07,0.42±0.04,0.35±0.03) and PCNA(control group 1.46±0.16;BTXA 0.50±0.05,0.59±0.05,0.37±0.03),inhibited the expression of PI3K(control group 0.98±0.06;BTXA 0.49±0.04,0.50±0.04,0.39±0.03) and the phosphorylation of AKT(control group 1.38±0.08;BTXA 0.97±0.06,0.60±0.04,0.29± 0.02),made cell cycle arrested in G1 phase,The difference was statistically significant (P＜0.05).Conclusion These results suggested BTXA inhibit proliferation via blocking the activation of PI3K/AKT signal pathway and down-stream related cell cycle related protein.关键词
肉毒毒素类/成纤维细胞/细胞周期/增生性瘢痕/磷脂酰肌醇3激酶/蛋白激酶B信号通路Key words
botulinum toxins/fibroblasts/cell cycle/hypertrohic scar/phosphatidylinositol 3 kinase/protein kinase B signal pathway分类
医药卫生引用本文复制引用
张雪,兰东,宁淑华,冉立伟,贾红侠,于思思,王晓军..A型肉毒毒素对增生性瘢痕成纤维细胞的抑制作用及机制[J].重庆医学,2017,46(5):580-582,585,4.基金项目
国家自然科学基金资助项目(81071571). （81071571）
