硫酸锌对皮瓣缺血再灌注损伤保护作用的研究

Study on the protective effects of ZnSO_4 on rat flaps with ischemia reperfusion injury

目的观察外源性锌对皮瓣缺血再灌注(ischemia-reperfusion,IR)损伤的保护作用,并探讨其机制。方法48只大鼠随机分为非-IR组I、R组和补锌-IR组。在大鼠以腹壁浅血管为蒂的岛状皮瓣缺血再灌注模型上,分别测定皮瓣组织中丙二醛(MDA)含量和髓过氧化物酶(MPO)活性。观察免疫组化切片中金属硫蛋白(metallothionein,MT)的表达,并对切片进行图像分析。应用透射电镜观察皮瓣缺血再灌注损伤后超微结构的改变,观察皮瓣成活率。结果补锌-IR组在再灌注1 h和24 h,皮瓣组织中MDA含量分别较IR组降低11.3%、33.2%(P<0.05),MPO活性分别较IR组降低14.2%、22.7%(P<0.05),MT含量分别较IR组高41.5%、44%(P<0.01)。在补锌-IR组掀起皮瓣即刻的标本中有一定量的MT表达。MT表达在皮瓣组织多种细胞的细胞浆中。补锌-IR组皮瓣的超微结构改变较IR组减轻,皮瓣成活率较IR组升高27.2%(P<0.05)。结论外源性锌能诱导皮瓣内MT产生,MT通过细胞保护作用对皮瓣缺血再灌注损伤产生一定的保护作用。

Objective To observe the protective role of the ectogenesis zinc in the rat flap with ischemia-reperfusion injury and study the mechanism. Methods An abdominal island flap was created in Wistar rats. 48 rats were randomly divided into three groups, 16 per group： the non-ischemia-reperfusion group, the ischemia-reperfusion group and the ischemia-reperfusion （IR） group treated with zinc. The content of malondialdehyde （MDA） and the activity of myeloperoxidase （MPO） were measured. The expression of metallothionein （MT） was observed, and the image analysis was performed. The ultrastructure changes of the skin flap with ischemia-reperfusion injury and the flap viability were observed. Results Compared with the IR group, at 1 h and 24 h of reperfusion, the level of MDA in the adding-zinc-IR group decreased 11.3% and 33.2% （P 〈 0.05）; the activity of MPO decreased 14.2% and 22.7% （P 〈 0.05）; the content of MT increased 41.5% and 44% （P〈 0.01） respectively. In the ischemia-reperfusion injury flaps, MT was located in the cytoplasm of many kinds of cells. The uhrastructure changes of the skin flap of the adding-zinc-IR group were slighter than those of the IR group. The flap viability in the adding-zinc-IR group increased 27.2% （ P 〈 0.05）. Conclusions MT could be induced by ectogenesis zinc in the flap of rats. The flap with ischemiareperfusion injury was protected by MT through protecting the cells in the flap.