医学分子生物学杂志 ›› 2022, Vol. 19 ›› Issue (4): 332-337.doi: 10.3870/j.issn.1672-8009.2022.04.011

• 论著 • 上一篇    下一篇

右美托咪定对口腔鳞癌细胞生长和运动能力的调节

  

  1. 1德阳市口腔医院口腔颌面外科 四川省德阳市, 618000  2成都市第七人民医院口腔科 成都市, 610000  3重庆医科大学附属第二医院整形美容与颌面外科 重庆市, 400000
  • 出版日期:2022-07-31 发布日期:2022-08-17

Effect of Dexmedetomidine on Growth and Motility of Oral Squamous Cell Carcinoma Cells

  1. 1Department of Oral and Maxillofacial Surgery, Deyang Stomatological Hospital, Deyang, Sichuan, 618000, China  2Department of Stomatology, Chengdu Seventh People’s Hospital, Chengdu, 610000, China  3Department of Plastic Surgery and Maxillofacial Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400000, China 
  • Online:2022-07-31 Published:2022-08-17

摘要: 目的 探究右美托咪定 ( dexmedetomidine, DEX) 对口腔鳞癌 ( oral squamous cell carcinoma, OSCC) 细胞生长和运动的调节作用。 方法 人 OSCC 细胞 CAL27 分为 DEX0、 5、 10 及 20 nmol / L 组。 运用 克隆形成实验和 BrdU 实验评估细胞增殖; Transwell 法检测细胞侵袭; 流式细胞术检测细胞凋亡率; ELISA 检测超氧化物歧化酶 (SOD) 和丙二醛 (MDA) 水平; 微管形成实验评估细胞微管形成能力; Western 印 迹检测血管内皮生长因子 (VEGF)、 纤连蛋白 ( FN)、 B 细胞淋巴瘤 2 ( Bcl-2) 和 Bcl-2 相关 X 蛋白 (Bax) 的表达。 结果 与对照组比较, DEX 处理可显著降低 CAL27 细胞克隆形成率和 BrdU 阳性细胞率, 减少侵袭细胞数和微管结节数, 下调 VEGF 和 FN 表达水平。 同时 DEX 处理可促进氧化应激, 提高 Bax / Bcl-2 比率。 结论 DEX 处理可抑制 CAL27 细胞增殖、 侵袭和微管形成能力, 并促进其氧化应激和凋亡。

关键词: 右美托咪定, 口腔鳞癌, 细胞凋亡, 血管内皮生长因子 

Abstract: Objective To investigate the effect of dexmedetomidine (DEX) on the growth and motility of oral squamous cell carcinoma (OSCC) cells. Methods Human OSCC cell line CAL27 were treated with DEX and were divided into groups of DEX 0, 5, 10 and 20 nmol / L. The proliferation of CAL27 cells was evaluated by colony formation assay and BrdU assay. Cell invasion was detected by transwell assay. Flow cytometry was employed to measure the apoptosis rate. The levels of superoxide dismutase ( SOD ) and malondialdehyde ( MDA ) in cells were determined by ELISA. The ability of cell microtubule formation was evaluated by the microtubule formation assay. Western blotting was performed to detect the expression levels of vascular endothelial growth factor (VEGF), fibronectin ( FN), B cell lymphoma 2 ( Bcl-2) and Bcl-2 associated X protein (Bax). Results DEX treatment significantly decreased the colony formation rate and BrdU positive cell rate, reduced the number of invasive cells and microtubule nodules, and down-regulated the expression levels of VEGF and FN in CAL27 cells when compared with the control group. Meanwhile, the treatment of DEX promoted the oxidative stress and increased the Bax / Bcl-2 ratio in cells. Conclusion DEX treatment can inhibit the proliferation, invasion and microtubule formation, and promote the oxidative stress and apoptosis in CAL27 cells.

Key words: dexmedetomidine, oral squamous cell carcinoma, apoptosis, vascular endothelial growth facto

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