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目的探讨磷脂酰肌醇3激酶(phosphatidylinositol 3 kinase,PI3K)-蛋白激酶B(protein kinase B,Akt)-叉头框蛋白(forkhead box O1,FOXO1)信号通路在盆腔脏器脱垂(pelvic organ prolapse,POP)中的表达及其在POP中的发病机制。方法选取2013年1月至2015年1月因POPⅢ度、Ⅳ度于武汉大学人民医院行全子宫切除术的患者20例(POP组)和同期因其他良性妇科疾病行全子宫切除术的患者20例(对照组),采用蛋白质免疫印记检测骶韧带组织中Akt、磷酸化蛋白激酶B(phosphorylation protein kinase B,p-Akt)、FOXO1、磷酸化(phosphorylation,p-)FOXO1、谷胱甘肽过氧化物酶(glutathione peroxidase1,GPX1)、锰超氧化物歧化酶(manganesesuperoxidedismutase,Mn-SOD)蛋白表达情况。结果 POP组较对照组,骶韧带组织中p-Akt/Akt、p-FOXO1/FOXO1表达比例明显上调,抗氧化蛋白GPX1、Mn-SOD表达下调。结论POP组织中PI3K-Akt-FOXO1信号通路被激活,并下调抗氧化蛋白GPX1、Mn-SOD表达,这一分子机制可能参与POP发生发展。
Objective To investigate the effect of the phosphatidylinositol 3 kinase (PI3K) - protein kinase B (Akt) - FOXO1 signaling pathway on pelvic organ prolapse , POP) and its pathogenesis in POP. Methods Twenty patients (POP group) who underwent hysterectomy due to POP Ⅲ degree and Ⅳ degree in Wuhan University People’s Hospital from January 2013 to January 2015 were enrolled in this study. Patients who underwent total hysterectomy for other benign gynecological diseases (Control group). The levels of Akt, phosphorylation protein kinase B (p-Akt), FOXO1, phosphorylation (p-) FOXO1, glutathione Glutathione peroxidase1 (GPX1) and manganese superoxide dismutase (Mn-SOD) protein expression. Results The expression of p-Akt / Akt, p-FOXO1 / FOXO1 in POP group was significantly higher than that in control group and sacral ligament tissues, and the expressions of GPX1 and Mn-SOD were down-regulated. Conclusion PI3K-Akt-FOXO1 signaling pathway is activated in POP and down-regulates the expression of antioxidant proteins GPX1 and Mn-SOD. This molecular mechanism may be involved in the development of POP.