子宫平滑肌RhoA/Rho激酶表达与宫缩乏力性产后出血的关系

摘要

Objective:To investigate the role of RhoA/Rho Kinase pathway in the postpartum hemorrhage by uterine atony. Methods:Sixty term delivery women were selected and divided into 2 groups:30 in postpartum hemorrhage caused by uterine atony and 30 in control group. The levels of contraction of myometrium were detected by RM6240 biological experimental system;the fluorescence quantitative RT-PCR and Western Blot were applied to detect the expression of RhoA, ROCK I , ROCK II in myometrium. Results: ①The levels of myometrium contraction in study group were lower than that of control group (P<0.01), when adding the Rho kinase inhibitor Y-27632 to strips,the levels of myometrium contraction in both group and control group were lower than untreated(P<0.01). ②The mRNA expression of RhoA,ROCK Ⅰ ,ROCK Ⅱ in study group were lower than control group (P< 0.05, P<0.01). ③The protein expressions of RhoA, ROCK Ⅰ , ROCKⅡin study group were lower than control group ( P< 0.05 ,P< 0.01). ④Both groups, Rho A mRNA and protein levels in myometrium were positively related to the levels of ROCK Ⅰ ,ROCKⅡ mRNA and protein. ⑤Both groups,RhoA,ROCK Ⅰ ,ROCKⅡ mRNA and protein levels in myometrium were positively related to the levels of myometrium contraction. Conclusions:Decreased RhoA/Rho Kinase Pathway expression in myometrium may be involved in the pathogenesis of postpartum hemorrhage by uterine atony.%目的:探讨产妇子宫平滑肌组织RhoA/Rho激酶表达与宫缩乏力性产后出血的关系.方法:选择30例宫缩乏力性产后出血产妇为病例组,同期无产后出血产妇30例为对照组.采用肌条等长张力测定法检测子宫平滑肌自发收缩活动力、加入Rho激酶抑制剂Y-27632后子宫平滑肌收缩活动力;采用实时荧光定量反转录聚合酶链反应(RT-PCR)法及蛋白质印迹法检测子宫平滑肌组织RhoA,ROCK Ⅰ和ROCKⅡmRNA及蛋白表达水平.结果:①病例组子宫平滑肌自发收缩活动力水平低于对照组,差异有统计学意义(P＜0.01)；病例组和对照组加入Y-27632后收缩活动力水平均低于加入前,差异有统计学意义(P＜0.01).②病例组子宫平滑肌组织RhoA,ROCK Ⅰ和ROCKⅡmRNA表达水平均低于对照组,差异均有统计学意义(P＜0.05或P＜0.01).③病例组子宫平滑肌组织RhoA,ROCK Ⅰ和ROCKⅡ蛋白表达水平均低于对照组,差异有统计学意义(P＜0.05或P＜0.01).④2组子宫平滑肌组织RhoA mRNA及蛋白与ROCK Ⅰ和ROCKⅡmRNA及蛋白表达水平均呈正相关.⑤2组子宫平滑肌组织RhoA,ROCK Ⅰ和ROCKⅡmRNA及蛋白水平均与子宫平滑肌基础收缩活动力水平呈正相关.结论:宫缩乏力性产后出血产妇子宫平滑肌组织RhoA,ROCK Ⅰ和ROCKⅡ水平均降低,且均与子宫平滑肌收缩活动力呈正相关,提示子宫平滑肌组织RhoA/Rho激酶信号通路表达降低可能是发生宫缩乏力性产后出血的分子机制之一.