Kössi Jyrki, Vähä-Kreula Marko, Peltonen Juha, Risteli Juha, Laato Matti
Department of Surgery, Päijät-Häme Central Hospital, Keskussairaalankatu 7, 15850 Lahti, Finland.
Arch Dermatol Res. 2004 May;295(12):521-6. doi: 10.1007/s00403-004-0461-8. Epub 2004 Mar 25.
Clinical observations have suggested that sugar and honey enhance granulation tissue formation and in vitro studies have shown that monosaccharide sugars stimulate mesenchymal and endothelial cells. In this study, the effects of glucose, fructose, galactose and mannose on type I and type III collagen gene expression and synthesis were studied in granulation tissue, hypertrophic scar and keloid fibroblast cultures. Glucose elevated both type I and type III collagen mRNAs in hypertrophic scar fibroblasts. Fructose increased type III collagen mRNA almost sevenfold in granulation tissue fibroblasts. Galactose caused an increase in type I and type III collagen mRNAs in granulation tissue fibroblasts and hypertrophic scar fibroblasts but, in contrast, mannose decreased type I and type III collagen levels in hypertrophic scar and keloid fibroblasts. Analysis of aminoterminal propeptides of type I and type III collagen (PINP and PIIINP) revealed that glucose decreased the amount of PINP in granulation tissue and keloid fibroblasts, whilst fructose decreased the amount in all the fibroblast cell lines studied. Galactose caused a decrease in the synthesis of type I collagen in all cell lines but a decrease was seen in type III collagen only in hypertrophic scar fibroblasts. Mannose decreased the amount of PINP in all cell lines but a decrease in the amount of PIIINP was seen only in granulation tissue fibroblasts. The effect of sugars on the ratio type I/type III collagen was negligible or decreasing with the exception of galactose, which increased the ratio in hypertrophic scar fibroblasts. The results suggest that glucose, fructose and galactose have no significant value in the stimulation of collagen synthesis in vitro. Mannose may have value in the prevention or treatment of abnormal scars.
临床观察表明,糖和蜂蜜可促进肉芽组织形成,体外研究显示单糖可刺激间充质细胞和内皮细胞。在本研究中,我们研究了葡萄糖、果糖、半乳糖和甘露糖对肉芽组织、肥厚性瘢痕和瘢痕疙瘩成纤维细胞培养物中I型和III型胶原基因表达及合成的影响。葡萄糖可提高肥厚性瘢痕成纤维细胞中I型和III型胶原mRNA水平。果糖可使肉芽组织成纤维细胞中III型胶原mRNA增加近7倍。半乳糖可使肉芽组织成纤维细胞和肥厚性瘢痕成纤维细胞中I型和III型胶原mRNA增加,但相反,甘露糖可降低肥厚性瘢痕和瘢痕疙瘩成纤维细胞中I型和III型胶原水平。对I型和III型胶原氨基末端前肽(PINP和PIIINP)的分析显示,葡萄糖可降低肉芽组织和瘢痕疙瘩成纤维细胞中PINP的含量,而果糖可降低所有研究的成纤维细胞系中PINP的含量。半乳糖可使所有细胞系中I型胶原合成减少,但仅在肥厚性瘢痕成纤维细胞中使III型胶原合成减少。甘露糖可降低所有细胞系中PINP的含量,但仅在肉芽组织成纤维细胞中使PIIINP含量减少。除半乳糖可增加肥厚性瘢痕成纤维细胞中I型/III型胶原比例外,糖类对I型/III型胶原比例的影响可忽略不计或呈下降趋势。结果表明,葡萄糖、果糖和半乳糖在体外刺激胶原合成方面无显著价值。甘露糖可能在预防或治疗异常瘢痕方面具有价值。