Rho/ROCK激酶信号通路在大鼠宫腔粘连中的作用

目的 复制宫腔粘连大鼠模型，探讨Rho/ROCK信号通路相关蛋白的表达及其在宫腔粘连中的作用机制。方法 SD大鼠宫腔注入0.5?ml 95%乙醇，复制宫腔粘连模型；对照组注入等量生理盐水。术后15?d观察两组子宫内膜形态学变化，免疫组织化学法检测子宫内膜角蛋白、波形蛋白、Rho（RhoA、RhoB、RhoC）、Rho激酶（ROCKI、ROCKII）及TGF-β1表达。结果 与对照组比较，模型组大鼠子宫内膜厚度变薄（P?<0.05）；两组腺体数目比较，模型组腺体数目减少（P?<0.05）；两组角蛋白比较，模型组表达下降（P?<0.05）；两组波形蛋白比较，差异无统计学意义（P?>0.05）；两组大鼠子宫内膜RhoA、RhoB、RhoC、ROCKI、ROCKII的表达比较，差异有统计学意义（P?<0.05），模型组均高于对照组；模型组大鼠子宫内膜TGF-β1的表达高于对照组（P?<0.05）。结论 注射无水乙醇可复制稳定的大鼠宫腔粘连动物模型，其Rho/ROCK信号通路处于激活状态，TGF-β1通过激活Rho/ROCK信号通路促使子宫内膜损伤后组织纤维化，参与宫腔粘连的发生、发展。

Role of Rho/ROCK kinase signaling pathway inuterine adhesion in rats

Objective To observe the expression of Rho/ROCK signaling pathway related proteins and explore its mechanism of action in intrauterine adhesion. Methods Rats were injected with anhydrous ethanol into uterine cavity to establish the model of uterine cavity adhesion. The control group was injected with the same amount of normal saline. Morphological changes of endometrium in the two groups were observed two weeks after surgery. The expression of keratin, vimentin, Rho (RhoA, RhoB, RhoC), Rho kinase (ROCKI, ROCKII) and TGF-beta 1 in the endometrium were detected by immunohistochemistry. Results Compared with the control group, the endometrium of the model group was thinner (P??0.05). In the model group, the expression of RhoA, RhoB, RhoC, ROCKI, ROCKII and TGF-beta 1 in endometrium of rats were higher than those in the control group with statistically significant differences (P?