脂肪组织来源的干细胞通过 p38/MAPK 通路抑制增生性瘢痕（HS）纤维化。
Adipose tissue-derived stem cells inhibit hypertrophic scar (HS) fibrosis via p38/MAPK pathway.
机构信息
Department of Breast and Thyroid Surgery, Renmin Hospital of Wuhan University, Wuhan, China.
Department of Orthopedic Sursery, West China Hospital, Chengdu, Sichuan, China.
出版信息
J Cell Biochem. 2019 Mar;120(3):4057-4064. doi: 10.1002/jcb.27689. Epub 2018 Sep 27.
OBJECTIVE
The current study was designed to investigate the effects and underlying mechanisms of adipose tissue-derived stem cells (ADSCs) on hypertrophic scar (HS) fibrosis.
METHOD
Real-time quantitative polymerase chain reaction (qRT-PCR) and Western blot analysis were performed to detect the expression of collagen I (Col1), collagen III (Col3), and α-smooth muscle actin (α-SMA) after fibroblasts and cultured HS tissues were treated with ADSC medium. All data were analyzed by using SPSS17.0 software. Statistical analysis was performed by Student t tests.
RESULTS
The in vitro study showed that ADSC medium decreased the expression of Col1, Col3, and α-SMA. In addition, the protein level of p-p38 was downregulated by ADSC medium treatment in a concentration dependent manner.
CONCLUSION
The current study demonstrated that ADSC could decrease collagen deposition and scar formation in in vitro experiments. The regulation of the p38/MAPK signaling pathway might play an important role in the process.
目的
本研究旨在探讨脂肪组织源性干细胞（ADSCs）对增生性瘢痕（HS）纤维化的作用及其潜在机制。
方法
采用实时定量聚合酶链反应（qRT-PCR）和 Western blot 分析检测 ADSC 培养基处理成纤维细胞和培养的 HS 组织后胶原 I（Col1）、胶原 III（Col3）和α-平滑肌肌动蛋白（α-SMA）的表达。所有数据均采用 SPSS17.0 软件进行分析。采用 Student t 检验进行统计学分析。
结果
体外研究表明，ADSC 培养基降低了 Col1、Col3 和 α-SMA 的表达。此外，ADSC 培养基处理呈浓度依赖性地下调 p-p38 的蛋白水平。
结论
本研究表明 ADSC 可减少体外实验中的胶原沉积和瘢痕形成。p38/MAPK 信号通路的调节可能在该过程中起重要作用。
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