缺血后处理激活自噬保护皮瓣机制研究

目的:缺血后处理皮瓣在临床上已经运用,开始相关研究探究缺血后处理对皮瓣保护机制。方法:健康成年新西兰大白兔,分为3组。A组为给予缺血后处理;B组为再灌注前5mi n给予自噬阻滞剂3-甲基腺嘌呤10μl+缺血后处理。C组,直接应用微血管夹阻断腹壁浅血管持续缺。6h后再灌。各组分别进行自噬指标Becl i n1、LC3免疫组化和皮瓣存活率检测。结果:新西兰大白兔完全存活。B、C组相比较,自噬Becl i n1、LC3免疫组化染色阳性细胞面积变化未见统计学差别(P>0.005)。实验组皮瓣存活面积比较,B与C相比较,无统计学意义(P>0.005),但是A与B、C相比较,上述指标两两之间都有统计学意义差别(P<0.005)。结论:缺血后处理对皮瓣再灌注损伤有保护作用,该作用可能和自噬激活有关。

Study on the mechanism of the autophagy protection activated by the ischemia postconditioning with skin flap

Objective The ischemia postconditioning is used for the protection of skin flap, a further study is done to explore the mechanism of the ischemia postconditioning on the skin flap. Methods The adult newzlend rabbits are divided into 3 group.A group is provided with ischemia postconiditoning,B group is provided with autophagy inhibitor 3-M ATP plus ischemia postconditio ning. C group is provided with direct ischemia with microvascular clamp.The study includes the respective test of the content of Beclinl,LC3 and the survival of skin flap of each group. Results The rabbits all survived.No difference existed between B and C group about content of Beclinl,LC3 （P〉 0.005）.No difference was found about the skin flap survival.But about the above three parameters,A group was found to have significance between B and C group. Conclusion Ischemia postconditioning can protect the skin flap which may be attributed to the role of the activation of autophagy.