Modulation of MCP-1, TGF-β1, and α-SMA Expressions in Granulation Tissue of Cutaneous Wounds Treated with Local Vitamin B Complex: An Experimental Study
IF 1.6
Q3 DERMATOLOGY
C. Martinelli-Kläy, L. O. Lunardi, C. Martinelli, T. Lombardi, E. G. Soares, C. Martinelli
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Abstract
Vitamin B complex can modulate the inflammatory response and activate wound healing. However, the action mechanisms involved in this process are still unclear. The aim of this study was to evaluate the effects of vitamin B complex on the modulation of monocyte chemotactic protein (MCP)-1, transforming growth factor (TGF)-β1, and α-smooth muscle actin (α-SMA) in granulation tissue growth. Cutaneous ulcers on Wistar rats were topically treated with vitamin B complex. MCP-1, TGF-β1, and α-SMA expressions were evaluated 24, 72, and 168 h after the treatment. Inflammatory cells were counted and collagen fibril staining was performed. After 24 h, more mononuclear cells (p ≤ 0.01) and a higher MCP-1 (p ≤ 0.05) and TGF-β1 (p ≤ 0.01) expression were observed. After 72 h, the number of fibroblasts and mononuclear cells (p ≤ 0.05) was elevated. After 168 h, an increased number of fibroblasts, myofibroblasts, and blood vessels (p ≤ 0.01) as well as a strong intensity of collagen fibril staining were seen. At that point, the cells presented a higher TGF-β1 expression (p ≤ 0.05), and the size of the ulcer area was decreased (p ≤ 0.01). We can conclude that vitamin B complex may stimulate a positive modulation of MCP-1, TGF-β1, and α-SMA expressions in granulation tissue of cutaneous ulcers. © 2014 S. Karger AG, Basel
局部维生素B复合物对皮肤创面肉芽组织中MCP-1、TGF-β1和α-SMA表达调节的实验研究
维生素B复合物可以调节炎症反应,促进伤口愈合。然而,这一过程所涉及的作用机制尚不清楚。本研究旨在探讨维生素B复合物对肉芽组织生长中单核细胞趋化蛋白(MCP)-1、转化生长因子(TGF)-β1和α-平滑肌肌动蛋白(α-SMA)的调节作用。用复合维生素B局部治疗Wistar大鼠皮肤溃疡。在治疗后24、72、168 h检测MCP-1、TGF-β1、α-SMA的表达。计数炎性细胞,进行胶原纤维染色。24 h后单核细胞增多(p≤0.01),MCP-1 (p≤0.05)、TGF-β1 (p≤0.01)表达增多。72h后,成纤维细胞和单核细胞数量显著升高(p≤0.05)。168 h后,成纤维细胞、肌成纤维细胞和血管数量增加(p≤0.01),胶原纤维染色强度增强。此时细胞TGF-β1表达升高(p≤0.05),溃疡面积减小(p≤0.01)。我们可以得出结论,维生素B复合物可能刺激皮肤溃疡肉芽组织中MCP-1、TGF-β1和α-SMA表达的正调节。©2014 S. Karger AG,巴塞尔
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