[1]张 雪,兰 东,宁淑华,等.基于TGF-β1/Smad通路探讨A型肉毒毒素对增生性瘢痕的抑制作用及机制[J].中国美容医学,2022,(5):93-97.
　ZHANG Xue,LAN Dong,NING Shuhua,et al.To Explore the Inhibitory Effect of Type A Botulinum Toxin on Hypertrophic Scar Based on TGF-1/Smad Pathway[J].Medical Aesthetics and Beauty,2022,(5):93-97.
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基于TGF-β1/Smad通路探讨A型肉毒毒素对增生性瘢痕的抑制作用及机制()
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《中国美容医学》[ISSN:1008-6445/CN:61-1347/R]

卷:
期数:
2022年5期
页码:
93-97
栏目:
出版日期:
2022-05-10

文章信息/Info

Title:
To Explore the Inhibitory Effect of Type A Botulinum Toxin on Hypertrophic Scar Based on TGF-1/Smad Pathway
文章编号:
1008-6455（2022）05-0093-04
作者:
张 雪; 兰 东; 宁淑华; 于思思
(首都医科大学附属北京朝阳医院皮肤与医疗美容科 北京 100043 )
Author(s):
ZHANG Xue; LAN Dong; NING Shuhua; YU Sisi
(Department of Dermatology and Plastic Surgery,Beijing Chao-Yang Hospital,Capital Medical University,Beijing 100043,China)
关键词:
A型肉毒毒素（BTXA）; TGF-β1/Smad通路; 增生性瘢痕; 机制
Keywords:
BTXA;  TGF- 1/Smad pathway;  hypertrophic scar;  mechanism
分类号:
R334+.5
文献标志码:
A
摘要:
目的：探讨A型肉毒毒素（BTXA）通过TGF-β1/Smad通路对增生性瘢痕成纤维细胞抑制作用及其机制。方法：体外培养增生性瘢痕成纤维细胞，采用0.2、0.4、0.8U/ml的BTXA处理成纤维细胞，分别作为0.2U/ml BTXA组、0.4U/ml BTXA组、0.8U/ml BTXA组，空白对照组不采用BTXA（0U/ml）处理，0.8 U/ml BTXA+TGF-β1组用0.8 U/ml BTXA和10 ng/ml的TGF-β1激活剂处理。甲基噻唑基四唑（MTT）法检测细胞活力；流式细胞术检测细胞凋亡率和细胞周期；蛋白质印迹法（Western blot）检测细胞周期蛋白（CyclinD1）、增殖细胞核抗原（PCNA）、Smad2/3、p-Smad2/3蛋白表达。结果：与空白对照组比较，0.2、0.4、0.8U/mlBTXA显著降低增生性瘢痕成纤维细胞活力和PCNA蛋白表达，差异有统计学意义（P＜0.05）。与空白对照组比较，0.2、0.4、0.8U/ml的BTXA显著提高增生性瘢痕成纤维细胞凋亡率（P＜0.05）。与空白对照组比较，0.2、0.4、0.8U/ml的BTXA显著升高增生性瘢痕成纤维细胞G0/G1期（P＜0.05）；显著降低细胞S期、G2/M期和Cyclin D1蛋白表达（P＜0.05）。与空白对照组比较，0.2、0.4、0.8U/ml的BTXA显著降低p-Smad2/3蛋白表达（P＜0.05）。与0.8U/ml BTXA组比较，0.8 U/ml BTXA+TGF-β1组显著升高增生性瘢痕成纤维细胞活力、S期、G2/M期和Cyclin D1、PCNA蛋白表达（P＜0.05）；显著降低细胞凋亡率和细胞G0/G1期（P＜0.05）。结论：BTXA通过抑制TGF-β1/Smad通路从而抑制增生性瘢痕成纤维细胞存活，为临床治疗提供了思路。
Abstract:
Objective To investigate the inhibitory effect of botulinum toxin type A (BTXA) on hypertrophic scar fibroblasts and its mechanism through TGF-β1/Smad pathway. Methods The hypertrophic scar fibroblasts were cultured in vitro, and the fibroblasts were treated with 0.2, 0.4, and 0.8 U/ml BTXA, respectively, as the 0.2 U/ml BTXA group, 0.4 U/ml BTXA group, and 0.8 U/ml BTXA group. The blank control group was not treated with BTXA (0 U/ml). The 0.8 U/ml BTXA+TGF-β1 group was treated with 0.8 U/ml BTXA and 10 ng/ml of TGF- β1 activator. Methylthiazolyltetrazole (MTT) method was used to detect cell viability; flow cytometry was used to detect cell apoptosis and cell cycle; Western blot was used to detect cell cycle protein (CyclinD1), proliferating cell nuclear antigen (PCNA), Smad2/ 3. p-Smad2/3 protein expression. Results Compared with the blank control group, 0.2, 0.4, 0.8 U/ml BTXA significantly reduced the viability of hypertrophic scar fibroblasts and the expression of PCNA protein (P ＜0.05). Compared with the blank control group, 0.2, 0.4, 0.8 U/ml BTXA significantly increased the apoptosis rate of hypertrophic scar fibroblasts (P＜0.05). Compared with the blank control group, 0.2, 0.4, 0.8 U/ml BTXA significantly increased the G0/G1 phase of hypertrophic scar fibroblasts (P＜0.05); significantly reduced the cell S phase, G2/M phase and Cyclin D1 protein expression (P＜0.05). Compared with the blank control group, 0.2, 0.4, 0.8 U/ml BTXA significantly reduced the expression of p-Smad2/3 protein (P＜0.05). Compared with 0.8 U/ml BTXA group, 0.8 U/ml BTXA+TGF-β1 group significantly increased the viability of hypertrophic scar fibroblasts, S phase, G2/M phase an d Cyclin D1, PCNA protein expression (P＜0.05), significantly reduce the rate of cell apoptosis and cell G0/G1 phase (P＜0.05). Conclusion BTXA inhibits the survival of hypertrophic scar fibroblasts by inhibiting the TGF- β1/Smad pathway
更新日期/Last Update: 2022-05-31