目的 探究右美托咪定對(duì)子宮內(nèi)膜癌細(xì)胞增殖、凋亡及Wnt/β-連環(huán)蛋白（β-catenin）通路的影響。方法 將Ishikawa、RL95-2細(xì)胞分為對(duì)照組，右美托咪定1、10、100 nmol/L組，右美托咪定（100 nmol/L）＋LiCl組。CCK-8法和EdU檢測(cè)細(xì)胞增殖，流式細(xì)胞術(shù)檢測(cè)細(xì)胞凋亡，Western blotting檢測(cè)增殖細(xì)胞核抗原（PCNA）、B淋巴細(xì)胞瘤-2蛋白（Bcl-2）、Bcl-2相關(guān)X蛋白（Bax）、β-連環(huán)蛋白（β-catenin）、c-Myc基因（c-Myc）、細(xì)胞周期蛋白D1（Cyclin D1）表達(dá)水平。構(gòu)建子宮內(nèi)膜癌裸鼠模型，分為對(duì)照組、右美托咪定組、右美托咪定＋LiCl組，測(cè)量腫瘤質(zhì)量與體積，蘇木精–伊紅（HE）染色觀察移植瘤組織形態(tài)，免疫組化法檢測(cè)移植瘤組織Ki-67、β-catenin蛋白表達(dá)。結(jié)果 與對(duì)照組相比，不同濃度右美托咪定處理后Ishikawa、RL95-2細(xì)胞吸光度（A）值、EdU陽性細(xì)胞率、遷移細(xì)胞數(shù)、侵襲細(xì)胞數(shù)、PCNA、Bcl-2、β-catenin、c-Myc、Cyclin D1蛋白表達(dá)顯著降低，凋亡率、Bax表達(dá)上升（P＜0.05）；與右美托咪定100 nmol/L組相比，右美托咪定＋LiCl組A值、EdU陽性細(xì)胞率、遷移細(xì)胞數(shù)、侵襲細(xì)胞數(shù)、PCNA、Bcl-2、β-catenin、c-Myc、Cyclin D1蛋白表達(dá)顯著升高，凋亡率、Bax表達(dá)下降（P＜0.05）。右美托咪定能抑制移植瘤質(zhì)量和體積，促進(jìn)腫瘤凋亡，降低β-catenin、Ki-67蛋白表達(dá)（P＜0.05）；LiCl能逆轉(zhuǎn)右美托咪定對(duì)移植瘤的抑制作用（P＜0.05）。結(jié)論 右美托咪定能抑制子宮內(nèi)膜癌細(xì)胞增殖，促進(jìn)凋亡，其作用機(jī)制可能與抑制Wnt/β-catenin信號(hào)通路有關(guān)。

Objective To investigate the impacts of dexmedetomidine on the proliferation, apoptosis, and Wnt/β-catenin pathway of endometrial cancer cells. Methods Ishikawa and RL95-2 cells were divided into control group, dexmedetomidine 1, 10, 100 nmol/L, and dexmedetomidine (100 nmol/L) + LiCl group. CCK-8 method and EdU were applied to detect cell proliferation, flow cytometry was applied to detect cell apoptosis, Western blotting was applied to detect the expression levels of PCNA, Bcl-2, Bax, β-catenin, c-Myc, and cyclin D1. An endometrial cancer nude mice model was constructed and divided into control group, dexmedetomidine group, and DEX + LiCl group, the mass and volume of the tumor are measured, HE staining was applied to observe the morphology of transplanted tumor tissue, immunohistochemical methods were applied to detect the expression of Ki-67 and β-catenin proteins in transplanted tumor tissue. Results Compared with control group, the A value, EdU positive cell rate, migration cell number, invasion cell number, PCNA, Bcl-2, β-catenin, c-Myc, and Cyclin D1 protein expression of Ishikawa and RL95-2 cells were obviously reduced after treatment with different concentrations of dexmedetomidine, the apoptosis rate and Bax expression increased (P < 0.05). Compared with dexmedetomidine 100 nmol/L group, the A value, EdU positive cell rate, migration cell number, invasion cell number, PCNA, Bcl-2, β-catenin, c-Myc, and Cyclin D1 protein expression in dexmedetomidine + LiCl group obviously increased, the apoptosis rate and Bax expression decreased (P < 0.05). Dexmedetomidine was able to inhibit the mass and volume of transplanted tumors, promote tumor apoptosis, and reduce the expression of β-catenin and Ki-67 proteins (P < 0.05), LiCl reversed the inhibitory effect of dexmedetomidine on transplanted tumors (P < 0.05). Conclusion Dexmedetomidine can inhibit proliferation and promote apoptosis of endometrial cancer cells, and its mechanism of action may be related to the inhibition of the Wnt/β-catenin signaling pathway.

R965

石家莊市科學(xué)技術(shù)研究與發(fā)展計(jì)劃項(xiàng)目（211200883）