Department of Gynecology, Ningbo Women and Children's Hospital, Ningbo, China.
Eur Rev Med Pharmacol Sci. 2019 Aug;23(16):6806-6812. doi: 10.26355/eurrev_201908_18719.
OBJECTIVE: To investigate the regulatory role of long non-coding ribonucleic acid (lncRNA) BRAF-activated non-coding RNA (BANCR) in rats with endometriosis (EMs) and its mechanism of action. MATERIALS AND METHODS: A total of 30 healthy, unmated, female Sprague-Dawley (SD) rats were selected and divided into sham-operation group, model group and lncRNA BANCR intervention group, and a rat model of EMs was established by means of autotransplantation. The volume of eutopic endometrium in each group of rats was measured, and hematoxylin and eosin (HE) staining was applied to detect the impacts on the pathological morphology of ectopic endometrial tissues in each group. The levels of vascular endothelial growth factor (VEGF), matrix metalloproteinase-2 (MMP-2) and MMP-9 in the rat serum were determined by virtue of enzyme-linked immunosorbent assay (ELISA), reverse transcription-polymerase chain reaction (RT-PCR) was performed to measure the messenger RNA (mRNA) levels of extracellular signal-regulated kinase (ERK) and mitogen-activated protein kinase (MAPK) in the uterine tissues in each group of rats, and Western blotting assay was adopted to detect the levels of phosphorylated ERK and MAPK proteins in the rat uterine tissues in each group. RESULTS: Compared with those in sham-operation group, the volume of eutopic endometrium in the rats was increased markedly, the pathological morphology was poorer, and the content of VEGF, MMP-2 and MMP-9 in the serum, the mRNA levels of ERK and MAPK in the uterine tissues, and the levels of phosphorylated ERK and MAPK proteins were elevated notably in model group. The rats in lncRNA BANCR intervention group had evidently decreased volume of eutopic endometrium, improved pathological morphology and significantly declined content of serum VEGF, MMP-2 and MMP-9, ERK and MAPK mRNA levels, and phosphorylated ERK and MAPK protein levels in the uterine tissues than those in model group. CONCLUSIONS: LncRNA BANCR inhibitor can repress the development of ectopic endometrial tissues by inhibiting the generation of angiogenic factors in the EMs focus, and its mechanism may be related to the inhibition on the ERK/MAPK signaling pathway.
目的：探讨长链非编码 RNA（lncRNA）BRAF 激活非编码 RNA（BANCR）在子宫内膜异位症（EMs）大鼠中的调控作用及其作用机制。
材料与方法：选择 30 只健康、未交配的雌性 Sprague-Dawley（SD）大鼠，分为假手术组、模型组和 lncRNA BANCR 干预组，采用自体移植法建立大鼠 EMs 模型。测量各组大鼠在位子宫内膜体积，苏木精-伊红（HE）染色检测各组异位子宫内膜组织病理形态学的影响。采用酶联免疫吸附试验（ELISA）测定大鼠血清中血管内皮生长因子（VEGF）、基质金属蛋白酶-2（MMP-2）和 MMP-9 的水平，逆转录-聚合酶链反应（RT-PCR）测定各组大鼠子宫组织中细胞外信号调节激酶（ERK）和丝裂原活化蛋白激酶（MAPK）的信使 RNA（mRNA）水平，采用 Western blot 检测各组大鼠子宫组织中磷酸化 ERK 和 MAPK 蛋白的水平。
结果：与假手术组相比，模型组大鼠在位子宫内膜体积明显增加，病理形态较差，血清中 VEGF、MMP-2 和 MMP-9 含量、子宫组织中 ERK 和 MAPK mRNA 水平以及磷酸化 ERK 和 MAPK 蛋白水平明显升高；lncRNA BANCR 干预组大鼠在位子宫内膜体积明显减少，病理形态明显改善，血清中 VEGF、MMP-2 和 MMP-9 含量、子宫组织中 ERK 和 MAPK mRNA 水平以及磷酸化 ERK 和 MAPK 蛋白水平明显降低。
结论：lncRNA BANCR 抑制剂可通过抑制 EMs 病灶中血管生成因子的产生来抑制异位子宫内膜组织的发生，其机制可能与抑制 ERK/MAPK 信号通路有关。
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