白芨胶载外源性碱性成纤维细胞生长因子促进伤口愈合的实验研究

摘要

背景:研究发现白芨凝胶可显著促进大鼠背部全层皮肤缺损创面肉芽组织、毛细血管的生长及创面组织血管内皮生长因子的表达,碱性成纤维细胞生长因子可显著促进兔背部全层皮肤缺损创面胶原纤维增生、毛细血管增多和扩张,但其在常温下易分解,影响功效发挥.目的:观察白芨联合外源性碱性成纤维细胞生长因子促进创面愈合的效果.方法:在40只新西兰大白兔背部制作全层皮肤缺损创面,随机分4组干预,白芨组创面外敷白芨,细胞因子组创面外喷碱性成纤维细胞生长因子液,联合组创面外敷白芨胶与碱性成纤维细胞生长因子混合物,生理盐水组以生理盐水冲洗创面,每组换药1次/d,直至创面愈合,记录创面愈合时间;创面损伤后第3,10天,检测创面愈合率;创面损伤后第7天,实时定量PCR及Western blot检测创面组织血管内皮生长因子、α-平滑肌肌动蛋白和Ⅰ型胶原基因及蛋白表达.结果与结论:①创面愈合时间:联合组创面愈合时间比生理盐水组提前了4.5 d(P < 0.05),比白芨组提前了3.0 d(P < 0.05),比细胞因子组提前了2.8 d(P < 0.05);②创面愈合率:联合组创面损伤后第3,10天的创面愈合率均高于其余3组(P < 0.05);③创面组织各基因及蛋白表达:联合组创面损伤后第7天的血管内皮生长因子、α-平滑肌肌动蛋白基因表达高于其余3组(P < 0.05),Ⅰ型胶原基因表达低于其余3组(P < 0.05);蛋白检测与基因检测结果一致;④结果表明:白芨联合外源性碱性成纤维细胞生长因子可促进创面愈合,其作用可能通过促进血管内皮生长因子表达、抑制Ⅰ型胶原表达来完成的.%BACKGROUND: Bletilla bletilla striata gelatin (BSG) is found to remarkably promote the growth of granulation tissue and capillary vessels, as well as the expression of vascular endothelial growth factor in the wound tissue in rabbits with full-thickness skin defect of the back. Basic fibroblast growth factor (bFGF) remarkably promotes the growth of collagen fibers and the growth and dilation of capillary vessels in the wound tissue in rabbits with full-thickness skin defect of the back. However, BSG is easy to decompose under normal temperature, affecting fulfillment of its functions. OBJECTIVE: To explore the effect of BSG carrying exogenous bFGF on wound healing. METHODS: Forty healthy rabbits were used to make animal models of full-thickness back skin defects, and then randomly divided into four groups, namely, group BSG+bFGF, group bFGF, group BSG and group saline. Rats in each group were subjected to the corresponding treatment once a day until the wound was completely healed. Wound healing time was recorded. Wound healing rate was detected at 3 and 10 days after modeling. Real-time PCR and western blot assay were used to detect the expression of vascular endothelial growth factor, α-smooth muscle actin and type I collagen at mRNA and protein levels at 7 days after modeling. RESULTS AND CONCLUSION: The wound healing time in the BSG+bFGF group was shortened by 4.5, 3.0 and 2.8 days as compared with the normal saline group, BSG group and bFGF group, respectively (P < 0.05). The wound healing rates in the BSG+bFGF group were also higher than those in the other groups at 3 and 10 days after modeling (P< 0.05). Findings from both PCR and western blot assay showed higher expression of vascular endothelial growth factor and α-smooth muscle actin and lower expression of type I collagen in the BSG+bFGF group than the other three groups at 7 days after modeling (P < 0.05). To conclude, BSG carrying exogenous bFGF can promote wound healing, and the underlying mechanism may be to promote vascular endothelial growth factor and inhibit type I collagen.