异丙酚对胶质瘤U87细胞增殖、侵袭、迁移及JAK2/STAT3通路的影响

摘要
图/表
参考文献
相关文章 (15)

全文: PDF (740 KB)
输出: BibTeX | EndNote (RIS)

摘要目的探讨异丙酚对胶质瘤U87细胞增殖、侵袭、迁移及Janus激酶2/信号转导子和转录激活子3(JAK2/STAT3)通路的影响。方法采用MTT法测定不同浓度的异丙酚对胶质瘤U87细胞和人正常星型胶质细胞HEB生长抑制作用,Transwell侵袭实验测定2、5、10 μM异丙酚对胶质瘤U87细胞体外侵袭能力的影响,划痕实验测定2、5、10 μM异丙酚对胶质瘤U87细胞体外迁移能力的影响,蛋白印迹法(WB)测定10 μM异丙酚对胶质瘤U87细胞JAK2/STAT3通路的影响。结果与对照组相比,5、10、25、50、100 μM异丙酚均能显著抑制胶质瘤U87细胞增殖,差异有统计学意义(P<0.05),后续选择2、5、10 μM异丙酚进行实验。与对照组相比,胶质瘤U87细胞经2、5、10 μM异丙酚处理后,侵袭能力显著降低,差异有统计学意义(P<0.05)。细胞划痕实验说明,胶质瘤U87细胞经2、5、10 μM异丙酚处理48 h后,迁移能力分别降低了(19.69±2.67)%、(41.41±3.28)%、(59.75±2.91)%,与对照组相比差异有统计学意义(P<0.05)。且胶质瘤U87细胞中JAK2蛋白磷酸化水平、STAT3蛋白磷酸化水平明显下调,与对照组相比差异有统计学意义(P<0.05)。结论异丙酚可能通过下调JAK2/STAT3信号传导通路相关蛋白表达,抑制胶质瘤U87细胞增殖、侵袭、迁移能力。

	服务

	把本文推荐给朋友
	加入我的书架
	加入引用管理器
	E-mail Alert
	RSS
	作者相关文章
	苏凯
	杨彦楠
	杨欣刚

关键词 ：异丙酚, 胶质瘤, 细胞增殖, 细胞侵袭, 细胞迁移

Abstract：Objective To study the effects of propofol on the proliferation, invasion, migration and Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway of glioma U87 cells. Methods MTT assay was used to determine the inhibitory effect of propofol at different concentrations on the growth of glioma U87 cells and human normal astrocyte HEB. Transwell invasion assay was used to determine the effects of 2 μM, 5 μM and 10 μM propofol on the invasive ability of glioma U87 cells in vitro. Scratch assay was used to determine the effects of 2 μM, 5 μM and 10 μM propofol on migration of glioma U87 cells in vitro, and the effect of propofol on JAK2/STAT3 pathway in U87 glioma cells was determined by Western blotting (WB). Results Compared with the control group, 5 μM, 10 μM, 25 μM, 50 μM and 100 μM propofol could significantly inhibit the proliferation of glioma U87 cells (P<0.05). Follow-up experiments were conducted with 2 μM, 5 μM and 10 μM propofol. Compared with the control group, the invasive ability of glioma U87 cells treated with 2 μM, 5 μM and 10 μM propofol decreased significantly (P<0.05). Scratch assay showed that the migration ability of U87 glioma cells treated with 2 μM, 5 μM and 10 μM propofol for 48 hours decreased by (19.69±2.67)%, (41.41±3.28)% and (59.75±2.91)% respectively, and there was significant difference between the two groups (P<0.05). The levels of JAK2 protein phosphorylation and STAT3 protein phosphorylation in U87 glioma cells treated with 2 μM, 5 μM and 10 μM propofol for 48 hours were significantly lower than those of the control group. Conclusions Propofol may inhibit the proliferation, invasion and migration of glioma U87 cells by down-regulating the expression of JAK2/STAT3 signal transduction pathway-related proteins.

Key words： propofol glioma cell proliferation cell invasion cell migration

收稿日期: 2020-11-20

ZTFLH:	R651.1
	R739.41

通讯作者: 杨欣刚,E-mail:yangxingang4621@sina.com

作者简介: 苏凯,硕士,医师。

引用本文:

苏凯, 杨彦楠, 杨欣刚. 异丙酚对胶质瘤U87细胞增殖、侵袭、迁移及JAK2/STAT3通路的影响[J]. 武警医学, 2021, 32(3): 197-200. SU Kai, YANG Yannan, YANG Xingang. Effects of propofol on proliferation, invasion, migration and JAK2/STAT3 pathway of glioma U87 cells. Med. J. Chin. Peop. Armed Poli. Forc., 2021, 32(3): 197-200.

链接本文:

http://journal08.magtechjournal.com/Jwk_wjyx/CN/ 或 http://journal08.magtechjournal.com/Jwk_wjyx/CN/Y2021/V32/I3/197

[1]	Zhou D X, Zhou D, Zhan S Q, et al. Inhibition of JMJD6 expression reduces the proliferation, migration and invasion of neuroglioma stem cells[J]. Neoplasma, 2017, 64(5):700-708.
[2]	Gupta A, Shaller N, McFadden K A. Pediatric thalamic gliomas:an updated review[J]. Arch Pathol Lab Med, 2017, 141(10):1316-1323.
[3]	李国亮, 王选重, 田沁森, 等. 脑胶质瘤综合治疗新进展[J]. 转化医学电子杂志, 2017,4(7):16-20.
[4]	吴亚琨, 王利宇, 孟庆刚, 等. 急性脑梗死溶栓后出现脑缺血再灌注损伤与炎性反应反应, 糖化清蛋白水平之间的关系以及异丙酚的保护效果分析[J]. 山西医药杂志, 2019, 48(1):9-13.
[5]	窦田友, 霍焱, 李君辉. 快速康复外科理念结合七氟醚、异丙酚全麻对老年乳腺癌术后苏醒时间及认知功能的影响[J]. 武警医学, 2018, 29(8): 766-769.
[6]	王菲, 喻文立, 贾莉莉, 等. 异丙酚通过抑制JAK/STAT通路减轻肝冷缺血再灌注大鼠肾损伤[J]. 中国病理生理杂志, 2016,32(11):2026-2030.
[7]	赵冀安, 聂文佳, 李卫,等. β干扰素联合全反式维甲酸通过抑制JAK2/STAT3信号通路抑制HepG2人肝癌细胞增殖并促进其凋亡[J]. 细胞与分子免疫学杂志, 2016,32(7):901-905.
[8]	Tang Y, Tong X, Li Y, et al. JAK2/STAT3 pathway is involved in the protective effects of epidermal growth factor receptor activation against cerebral ischemia/reperfusion injury in rats[J]. Neurosci Lett, 2018,662 (1):219-226.
[9]	Pan I W, Ferguson S D, Lam S. Patient and treatment factors associated with survival among adult glioblastoma patients: a USA population-based study from 2000-2010[J]. Clin Neurosci,2015, 22(10):1575-1581.
[10]	徐然, 仇文进, 陈正新,等. FOXP2调控PI3K/Akt信号通路抑制胶质瘤的侵袭[J]. 南京医科大学学报(自然科学版), 2017,37(5):45-49.
[11]	Huang W Y, Ding X P, Ye H B, et al. Hypoxia enhances the migration and invasion of human glioblastoma U87 cells through PI3K/Akt/mTOR/HIF-1α pathway[J]. NeuroReport, 2018, 29(18):1578-1585.
[12]	Yang N, Liang Y, Yang P, et al. Propofol suppresses LPS-induced nuclear accumulation of HIF-1α and tumor aggressiveness in non-small cell lung cancer[J]. Oncol Rep, 2017,37(5):2611-2619.
[13]	Xu J, Xu W, Zhu J. Propofol suppresses proliferation and invasion of glioma cells by upregulating microRNA-218 expression[J]. Mol Med Rep, 2015, 12(4):4815-4820.
[14]	张永强, 刘俊, 陈胜阳, 等. 异丙酚影响基质金属蛋白酶对肺腺癌细胞株增殖侵袭能力的作用[J]. 实用医学杂志, 2018,34(3):357-361.
[15]	周桥灵, 刘洪珍, 杨敏清, 等. PI3K/Akt信号通路在异丙酚抑制人肝癌细胞侵袭中的作用[J]. 中华麻醉学杂志, 2018,38(1):110-113.
[16]	闵娜, 胡强夫, 张韶南, 等. 异丙酚通过Wnt/β-catenin信号通路对HepG2细胞表达抑制作用的研究[J]. 实用糖尿病杂志, 2017,13(3):46-47.
[17]	王洪海, 周颖璨, 周德生, 等. JAK2/STAT3通路在脑缺血再灌注损伤炎性反应中的作用[J]. 西部医学, 2017,29(2):172-178.
[18]	郭佳培, 郭彬, 李雷雷,等. 青蒿素通过抑制JAK2/STAT3信号通路诱导肝癌细胞凋亡[J]. 山西医科大学学报, 2017,48(2):5-8.
[19]	胡兵, 王鸿梅, 初建设. 微小RNA-375对鼻咽癌细胞侵袭迁移及JAK2/STAT3信号通路的影响[J]. 临床肿瘤学杂志, 2017,22(8):12-16.