Huiyang Shengji Extract Improve Chronic Nonhealing Cutaneous through the TGF-β1/Smad3 Signaling Pathway

被引:2
作者
Lin, Yan [1 ]
He, Xiujuan [1 ]
Xie, Xinran [1 ]
Liu, Qingwu [1 ,2 ]
Chen, Jia [1 ,2 ]
Li, Ping [1 ,2 ]
机构
[1] Capital Med Univ, Beijing Inst TCM, Beijing Hosp Tradit Chinese Med, 23 Gallery Backst, Beijing 100010, Peoples R China
[2] Beijing Univ Chinese Med, 11 North Third Ring Rd, Beijing 100029, Peoples R China
基金
中国国家自然科学基金;
关键词
DIABETES-MELLITUS; MACROPHAGES; EXPRESSION; FIBROBLASTS; PHENOTYPE; FIBROSIS; WOUNDS; METALLOPROTEINASES; ACTIVATION; CELLS;
D O I
10.1155/2021/8881565
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
Chronic nonhealing cutaneous wounds are a thorny problem in the field of surgery because of their prolonged and unhealed characteristics. Huiyang Shengji extract (HSE) is an extract of traditional Chinese medicine prescription for treating chronic wounds. This study aims to investigate the regulation of M1 macrophages on fibroblast proliferation and secretion and the intervention mechanism of Huiyang Shengji extract. We found that the effects of HSFs stimulated with paracrine factors from M1 macrophages were as follows: the proliferation of HSFs was reduced, the expression of MKI-67 was downregulated, and the content and gene expression of the inflammation factors and fibroblast MMPs were increased, while the content and gene expression of TIMP-1 are decreased, the content of human fibroblasts secreting type I collagen (COL1A1) and type III collagen (COL3A1) was decreased, and the TGF-beta 1/Smad3 signaling pathway was inhibited. Interestingly, HSE inhibited these effects of M1 macrophages on human fibroblasts after the intervention, and the inhibitory effect was related to the concentration. In conclusion, M1 macrophages caused changes in HSFs and secretion, while HSE has a specific regulatory effect on the proliferation and secretion of fibroblasts caused by M1 macrophages.
引用
收藏
页数:12
相关论文
共 32 条
[1]   Impaired TGF-β signaling and a defect in resolution of inflammation contribute to delayed wound healing in a female rat model of type 2 diabetes [J].
Al-Mulla, Fahd ;
Leibovich, Samuel J. ;
Francis, Issam M. ;
Bitar, Milad S. .
MOLECULAR BIOSYSTEMS, 2011, 7 (11) :3006-3020
[2]   Identification of a myofibroblast-specific expression signature in skin wounds [J].
Bergmeier, Vera ;
Etich, Julia ;
Pitzler, Lena ;
Frie, Christian ;
Koch, Manuel ;
Fischer, Matthias ;
Rappl, Gunter ;
Abken, Hinrich ;
Tomasek, James J. ;
Brachvogel, Bent .
MATRIX BIOLOGY, 2018, 65 :59-74
[3]   Metalloproteinases and Wound Healing [J].
Caley, Matthew P. ;
Martins, Vera L. C. ;
O'Toole, Edel A. .
ADVANCES IN WOUND CARE, 2015, 4 (04) :225-234
[4]   Smad3 Signaling Critically Regulates Fibroblast Phenotype and Function in Healing Myocardial Infarction [J].
Dobaczewski, Marcin ;
Bujak, Marcin ;
Li, Na ;
Gonzalez-Quesada, Carlos ;
Mendoza, Leonardo H. ;
Wang, Xiao-Fan ;
Frangogiannis, Nikolaos G. .
CIRCULATION RESEARCH, 2010, 107 (03) :418-U176
[5]  
Han X, 2016, BASED UPLCQ TOF MSE
[6]   Direct contact between human peripheral blood mononuclear cells and renal fibroblasts facilitates the expression of monocyte chemoattractant protein-1 [J].
Hao, LR ;
Okada, H ;
Kanno, Y ;
Inoue, T ;
Kobayashi, T ;
Watanabe, Y ;
Strutz, F ;
Müller, GA ;
Suzuki, H .
AMERICAN JOURNAL OF NEPHROLOGY, 2003, 23 (04) :208-213
[7]  
He XJ, 2018, INT J CLIN EXP MED, V11, P11690
[8]   Cell-cell signaling in co-cultures of macrophages and fibroblasts [J].
Holt, Dolly J. ;
Chamberlain, Lisa M. ;
Grainger, David W. .
BIOMATERIALS, 2010, 31 (36) :9382-9394
[9]   Human umbilical cord mesenchymal stem cell-derived exosomes suppress dermal fibroblasts-myofibroblats transition via inhibiting the TGF-β1/Smad 2/3 signaling pathway [J].
Hu, Jian ;
Chen, Yuanwen ;
Huang, Yubin ;
Su, Yongsheng .
EXPERIMENTAL AND MOLECULAR PATHOLOGY, 2020, 115
[10]   Matrix metalloproteinases: The sculptors of chronic cutaneous wounds [J].
Krishnaswamy, Venkat Raghavan ;
Mintz, Dvir ;
Sagi, Irit .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, 2017, 1864 (11) :2220-2227