Effects of Botulinum Toxin Type A on Proliferation, Apoptosis and ERK/MAPK Signaling Pathway of Hypertrophic Scar Fibroblasts
10.11969/j.issn.1673-548X.2017.07.007
- VernacularTitle:A型肉毒毒素对增生性瘢痕成纤维细胞增殖、凋亡及对ERK/MAPK信号通路的影响
- Author:
Li SHEN
;
Yang YU
;
Shaolin MA
- Keywords:
Botulinum toxin type A;
Hypertrophic scar;
Fibroblast;
ERK;
MAPK
- From:
Journal of Medical Research
2017;46(7):26-29,74
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of botulinum toxin type A on the proliferation,apoptosis and ERK/MAPK signaling pathway of human hypertrophic scar fibroblasts in vitro.Methods Fibroblasts were isolated from human hypertrophic scar and cultured by tissue explant method.The cells were divided into control and botulinum toxin type A groups.The botulinum toxin group A was cultured in DMEM medium containing 0.4U/L botulinum toxin type A.The control group was cultured with DMEM alone.Cell proliferation was measured by CCK8 kit at days 1,3,5 and 7 and compared within groups.Apoptosis of fibroblasts was detected by flow cytometry which treated with botulinum toxin and control group.Western blot was used to detect the relative expression of collagen Ⅰ,p-ERK1/2 and total ERK protein in fibroblasts of control,botulinum toxin type A and U0126 groups.Results Botulinum toxin type A could significantly inhibit the proliferation of fibroblasts,the number of cells was only 68.9％ in the control group at 7th days.The apoptotic rate of botulinum toxin type A was 35.9％,which was significantly higher than that of the control group.ERK 1/2 protein expression in the three groups was not significantly different (P ＞ 0.05),while p-ERK 1/2 expression in the control group was still significantly higher,but the p-EKR 1/2 in botulinum toxin type A and U0126 group was significantly inhibited.Collagen Ⅰ was highly expressed in the control group,which was significantly higher than that in the botulinum toxin type A and U0126 groups (P ＜ 0.05).Conclusion Botulinum toxin type A can inhibit the ERK/MAPK signaling pathway and increased fibroblasts apoptosis,decreased proliferation activity and collagen Ⅰ secretion.
