CAJ | 학술논문

目的研究巨噬细胞及粒巨细胞-集落刺激因子(GM-CSF)对大鼠腹壁动脉穿支(deep epigastric perforator,DEP)皮瓣模型的影响.方法建立SD大鼠DEP皮瓣模型,分别给予大鼠GM-CSF(Ⅰ组)、腹腔巨噬细胞(Ⅱ组)、GM-CSF联合巨噬细胞(Ⅲ组)及乍理盐水(Ⅳ组).术后第7天取皮瓣检测成活而积、组织学观察、微血管密度(MVD)、皮瓣内胶原含量.结果皮瓣成活率Ⅰ组(53.08%±8.76%)和Ⅱ组(47.95%±4.92%)间无差异,均高于Ⅳ组(43.28%±5.27%)而低于Ⅲ组(61.68%±6.60%),P<0.05.皮瓣MVD Ⅰ组(24.82±4.18)和Ⅱ组(24.30±3.02)间差异无统计学意义,均显著高于Ⅳ组(21.37±2.65),低于Ⅲ组(29.82±4.74).胶原含量Ⅰ组(17.25%±2.85%)高于Ⅳ组(14.41%±2.89%),P<0.05.Ⅱ组(12.69%±3.55%)稍低于Ⅳ组.Ⅲ组(20.31%±3.01%)较Ⅰ组显著增高,P<0.05.结论重组大鼠GM-CSF和巨噬细胞均能够促进大鼠DEP皮瓣成活,联合应用可发挥协同作用促进皮瓣存活、血管生成以及胶原沉积.
목적 연구거서세포급립거세포-집락자격인자(GM-CSF)대대서복벽동맥천지(deep epigastric perforator,DEP)피판모형적영향.방법 건립SD대서DEP피판모형,분별급여대서GM-CSF(Ⅰ조)、복강거서세포(Ⅱ조)、GM-CSF연합거서세포(Ⅲ조)급사리염수(Ⅳ조).술후제7천취피판검측성활이적、조직학관찰、미혈관밀도(MVD)、피판내효원함량.결과 피판성활솔Ⅰ조(53.08%±8.76%)화Ⅱ조(47.95%±4.92%)간무차이,균고우Ⅳ조(43.28%±5.27%)이저우Ⅲ조(61.68%±6.60%),P<0.05.피판MVD Ⅰ조(24.82±4.18)화Ⅱ조(24.30±3.02)간차이무통계학의의,균현저고우Ⅳ조(21.37±2.65),저우Ⅲ조(29.82±4.74).효원함량Ⅰ조(17.25%±2.85%)고우Ⅳ조(14.41%±2.89%),P<0.05.Ⅱ조(12.69%±3.55%)초저우Ⅳ조.Ⅲ조(20.31%±3.01%)교Ⅰ조현저증고,P<0.05.결론 중조대서GM-CSF화거서세포균능구촉진대서DEP피판성활,연합응용가발휘협동작용촉진피판존활、혈관생성이급효원침적.
Objective To study the effect of macrophage, its stimulating factor, granulocyte macrophage colony-stimulating factor (GM-CSF), the combination of GM-CSF and macrophage on the survival of rat deep epigastric perforator flap (DEP). Methods The stable animal model of DEP flap in Sprague-Dawley rat mimicing human deep inferior epigastric perforator flap in breast reconstruction was established. The rats were treated with subcutaneous injection of recombined rat GM-CSF or rat peritoneal macrophages, respectively, or combination of GM-CSF/ Macrophages. Normal saline was used as parallel negative control. The rats were sacrificed and flap specimens were harvested on day 7 after operation, the flaps survival area were measured by the method of rubbings and the survival proportion of flaps were calculated, Von Will brand factor were detected by immunohistochemistry and microvessel density (MVD), and were calculated with microscopic study, and collagen were stained and quantified by Masson staining. Results Survival proportion of flaps in group GM-CSF (53.08% ± 8. 76% ) was not different with that in macrophages group (47. 95% ± 4. 92% ), and both of these two groups were significantly higher than parallel negative control group (43.28% ± 5.27% ) but significantly lower than combination GM-CSF/ macrophages group ( 61.68% ± 6. 60% ). For MVD, flap in GM-CSF group ( 24. 82 ± 4. 18 ) was not significantly different with macrophages group (24.30 ± 3.02 ), and both of these two groups were significantly higher than group parallel negative control (21.37 ± 2.65 ) but significantly lower than combination GM-CSF/macrophages group ( 29. 82 ± 4. 74). Collagen deposition in the flaps in GM-CSF group (17. 25% ± 2. 85% ) were significantly higher than parallel negative control group (14.41% ± 2. 89% ), macrophages group ( 12. 69% ± 3.55% ) were lower than parallel negative control group but there was no significant difference. That in combination GM-CSF/macrophages group (20.31% ± 3.01% )was significantly higher than GM-CSF group ( P < 0. 05 ). Conclusion Treatment with rat GM-CSF or macrophage can significantly promote the survival of the flaps. Combined application of GM-CSF and macrophage could synergetically promote the survival of the flaps, the vasculogenesis and the collagen deposition.