ERK通路参与雌二醇减轻皮瓣缺血再灌注损伤的机制研究

被引:8
作者
金乾衡
巨积辉
侯瑞兴
徐磊
刘跃飞
机构
[1] 苏州,苏州大学附属瑞华医院手外科
关键词
雌二醇; 外科皮瓣; 缺血再灌注损伤; 细胞凋亡; 细胞外信号调节激酶通路;
D O I
暂无
中图分类号
R622 [整形手术学];
学科分类号
100224 [整形外科学];
摘要
目的研究雌二醇对大鼠腹部轴型皮瓣缺血再灌注(I/R)损伤的影响, 并探讨其与细胞外信号调节激酶(ERK)通路的关系, 为雌二醇应用于临床治疗I/R损伤提供理论基础。方法取健康雄性Wistar大鼠50只, 随机分为对照组(Ⅰ组)、I/R组(Ⅱ组)、生理盐水组(Ⅲ组)、雌二醇组(Ⅳ组)及抑制剂组(Ⅴ组), 每组10只。于大鼠左下腹切取3.0 cm×6.0 cm以腹壁浅动脉为蒂的轴型皮瓣, 用无创显微血管夹夹闭腹壁浅动静脉, 以形成大鼠腹部皮瓣I/R模型。术后2、4、6 d观察皮瓣变化情况, 术后第七天测定皮瓣成活率。取皮瓣组织进行HE染色组织学观察, TUNEL染色检测细胞凋亡指数。Western blot检测皮瓣组织ERK、p-ERK、MKP-1蛋白表达水平。结果Ⅳ组皮瓣成活率明显高于Ⅱ、Ⅲ、Ⅴ组, Ⅴ组皮瓣成活率高于Ⅱ、Ⅲ组(P<0.05);Ⅳ组ERK、p-ERK蛋白表达水平明显高于Ⅱ、Ⅲ、Ⅴ组(P<0.05), 而MKP-1蛋白表达水平明显低于Ⅱ、Ⅲ、Ⅴ组(P<0.05);细胞凋亡指数Ⅰ和Ⅳ组较其他组明显低(P<0.05)。结论雌二醇可能通过抑制MKP-1介导ERK磷酸化表达变化, 从而抑制细胞凋亡, 使皮瓣I/R损伤减轻。
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