Uysal A Cagri, Mizuno Hiroshi, Tobita Morikuni, Ogawa Rei, Hyakusoku Hiko
Tokyo, Japan From the Department of Plastic and Reconstructive Surgery, Nippon Medical School.
Plast Reconstr Surg. 2009 Sep;124(3):804-815. doi: 10.1097/PRS.0b013e3181b17bb4.
Advances in the treatment of reperfusion injury have created an opportunity for plastic surgeons to apply these treatments to flaps and implanted tissues. The authors examined the direct and indirect effects of adipose-derived stem cells on ischemia-reperfusion injury on a skin flap model to determine the in vivo differentiation of adipose-derived stem cells to endothelial cells; the levels of vascular endothelial growth factor (VEGF), transforming growth factor-beta, and fibroblast growth factor; and the ultrastructural changes apparent with scanning electron microscopy to clarify the initial events and the following cascades.
Two identical cranial based random flaps with a dimension of 1 x 5 cm were elevated on the dorsums of 20 ICR mice. The left flap was designated as the control and the right flap was injected with adipose-derived stem cells. The flaps were then subjected to 6 hours of ischemia by clamping the pedicle, and then reperfusion.
The mean viable flap length in the control and experimental groups was 15.2 +/- 3.4 mm and 24.4 +/- 2.9 mm, respectively. The mean viable flap area in the control and experimental groups was 12.9 +/- 4.1 mm and 21.8 +/- 3.7 mm, respectively. The in vivo differentiation of adipose-derived stem cells to endothelial cells was observed. The immunohistochemical stainings, VEGF, transforming growth factor-beta, and fibroblast growth factor revealed increased levels in the experimental groups. Scanning electron microscopy indicated mild injury in the experimental group.
The adipose-derived stem cells could prevent ischemia-reperfusion injury, mainly by regulating the growth factors. Although VEGF was the foremost inhibitor of injury, the overall cascade was enhanced by adipose-derived stem cells, with the help of the other growth factors.
再灌注损伤治疗方面的进展为整形外科医生将这些治疗方法应用于皮瓣和植入组织创造了机会。作者在皮瓣模型上研究了脂肪干细胞对缺血再灌注损伤的直接和间接影响,以确定脂肪干细胞在体内向内皮细胞的分化情况;血管内皮生长因子(VEGF)、转化生长因子-β和成纤维细胞生长因子的水平;以及扫描电子显微镜下明显的超微结构变化,以阐明初始事件和后续级联反应。
在20只ICR小鼠的背部掀起两个尺寸为1×5 cm的相同颅基随机皮瓣。将左侧皮瓣指定为对照组,右侧皮瓣注射脂肪干细胞。然后通过夹闭蒂部使皮瓣缺血6小时,随后再灌注。
对照组和实验组皮瓣的平均存活长度分别为15.2±3.4 mm和24.4±2.9 mm。对照组和实验组皮瓣的平均存活面积分别为12.9±4.1 mm和21.8±3.7 mm。观察到脂肪干细胞在体内向内皮细胞的分化。免疫组织化学染色显示,实验组中VEGF、转化生长因子-β和成纤维细胞生长因子水平升高。扫描电子显微镜显示实验组有轻度损伤。
脂肪干细胞可主要通过调节生长因子来预防缺血再灌注损伤。虽然VEGF是损伤的主要抑制因子,但在其他生长因子的帮助下,脂肪干细胞增强了整体级联反应。