[1]齐少霞,杨栋宝,周翼,等.丙泊酚对脂多糖诱导肝癌细胞炎症反应、增殖、黏附、侵袭的影响及机制[J].新乡医学院学报,2023,40(8):712-720.[doi:10.7683/xxyxyxb.2023.08.003]
　QI Shaoxia,YANG Dongbao,ZHOU Yi,et al.Effect and mechanism of propofol on lipopolysaccharide-induced inflammation response,proliferation,adhesion and invasion of hepatocellular carcinoma cells[J].Journal of Xinxiang Medical University,2023,40(8):712-720.[doi:10.7683/xxyxyxb.2023.08.003]
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丙泊酚对脂多糖诱导肝癌细胞炎症反应、增殖、黏附、侵袭的影响及机制
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《新乡医学院学报》[ISSN:1004-7239/CN:41-1186/R]

卷:
40卷
期数:
2023年8
页码:
712-720
栏目:
基础研究
出版日期:
2023-08-05

文章信息/Info

Title:
Effect and mechanism of propofol on lipopolysaccharide-induced inflammation response,proliferation,adhesion and invasion of hepatocellular carcinoma cells
作者:
齐少霞; 杨栋宝; 周翼; 武倩; 王晓东
（沧州中西医结合医院麻醉二科，河北　沧州　061000）
Author(s):
QI Shaoxia; YANG Dongbao; ZHOU Yi; WU Qian; WANG Xiaodong
(The Second Department of Anesthesiology,Cangzhou Hospital of Integrated Chinese and Western Medicine,Cangzhou 061000,Hebei Province,China)
关键词:
肝癌; 丙泊酚; 脂多糖; 增殖; 凋亡; 黏附; 侵袭; 上皮间质转化
Keywords:
liver cancer; propofol; lipopolysaccharide; proliferation; apoptosis; adhesion; invasion; epithelial-mesenchymal transition
分类号:
R735.7
DOI:
10.7683/xxyxyxb.2023.08.003
文献标志码:
A
摘要:
目的　探讨丙泊酚对脂多糖（LSP）诱导的人肝癌细胞炎症反应、增殖、凋亡、黏附、侵袭的影响及机制。
方法　将对数生长期肝癌MHCC97H细胞按随机数字表法分为对照组、LPS组和低剂量丙泊酚、中剂量丙泊酚、高剂量丙泊酚组。对照组细胞不做干预；LPS组细胞给予1 mg·L-1 LPS干预；低剂量丙泊酚组、中剂量丙泊酚组和高剂量丙泊酚组均给予1 mg·L-1 LPS干预24 h后，再分别给予12.5、25.0和50.0 μmol·L-1丙泊酚干预。采用酶联免疫吸附试验检测各组细胞培养液中炎症因子白细胞介素1β（IL-1β）和肿瘤坏死因子-α（TNF-α）表达水平，采用细胞计数试剂盒-8测定各组细胞活力，采用5-乙炔基-2′脱氧尿嘧啶核苷法检测各组细胞增殖情况，采用Hoechst 33258染色法检测各组细胞凋亡情况，采用细胞黏附实验测定各组黏附细胞数，采用Transwell小室检测各组细胞的侵袭能力，采用蛋白免疫印迹法测定细胞周期素D1（Cyclin D1）、caspase-3、E-钙黏蛋白（E-cadherin）、N-钙黏蛋白（N-cadherin）、波形蛋白（Vimentin）和纤连蛋白（FN）表达水平。
结果　LPS组IL-1β水平、TNF-α水平、细胞活力、细胞增殖率、黏附细胞数、侵袭细胞数及Cyclin D1、N-cadherin、Vimentin和FN水平显著高于对照组（P<0.05），细胞凋亡率和caspase-3、E-cadherin 水平显著低于对照组（P<0.05）。中剂量丙泊酚组、高剂量丙泊酚组TNF-α水平、细胞活力、细胞增殖率、黏附细胞数、侵袭细胞数及Cyclin D1、N-cadherin、Vimentin水平显著低于对照组（P<0.05），细胞凋亡率、caspase-3、E-cadherin蛋白表达水平显著高于对照组（P<0.05）；中剂量丙泊酚组、高剂量丙泊酚组与对照组IL-1β水平比较差异无统计学意义（P>0.05）；高剂量丙泊酚组FN水平显著低于对照组（P<0.05），中剂量丙泊酚组与对照组FN蛋白表达水平比较差异无统计学意义（P>0.05）。 低剂量丙泊酚组细胞侵袭数、E-cadherin水平显著低于对照组，Cyclin D1水平显著高于对照组（P<0.05）；低剂量丙泊酚组与对照组细胞活力、细胞增殖率、细胞凋亡率、黏附细胞数比较差异无统计学意义（P>0.05）。 中剂量丙泊酚组、高剂量丙泊酚组IL-1β水平、TNF-α水平、细胞活力、细胞增殖率、黏附细胞数及侵袭细胞数、Cyclin D1、N-cadherin、Vimentin和FN水平显著低于LPS组和低剂量丙泊酚组，细胞凋亡率及caspase-3、E-cadherin水平显著高于LPS组和低剂量丙泊酚组（P<0.05）。高剂量丙泊酚组TNF-α水平、黏附细胞数、侵袭细胞数及N-cadherin和FN水平显著低于中剂量丙泊酚组，细胞凋亡率、E-cadherin蛋白表达水平显著高于中剂量丙泊酚组（P<0.05）；高剂量丙泊酚组与中剂量丙泊酚组细胞活力、细胞增殖率及IL-1β、Cyclin D1和caspase-3、Vimentin水平比较差异无统计学意义（P>0.05）。 低剂量丙泊酚组细胞活力、细胞增殖率、黏附细胞数、侵袭细胞数、Cyclin D1、N-cadherin、Vimentin和FN水平显著低于LPS组（P<0.05），细胞凋亡率及caspase-3、E-cadherin水平显著高于LPS组（P<0.05）；低剂量丙泊酚组与LPS组IL-1β和TNF-α表达水平比较差异无统计学意义（P>0.05）。
结论　丙泊酚可通过抑制上皮间质转化进程缓解LPS诱导肝癌细胞的炎症反应，抑制肝癌细胞增殖、黏附和侵袭，诱导肝癌细胞凋亡。
Abstract:
Objective　To investigate the effect and mechanism of propofol on lipopolysaccharide(LSP)-induced inflammatory response,proliferation,apoptosis,adhesion and invasion of human hepatocellular carcinoma cells.
Methods　Hepatocellular carcinoma MHCC97H cells in logarithmic growth phase were divided into control group,LPS group and low-dose propofol group,medium-dose propofol group and high-dose propofol group according to the random number table method.The cells in the control group were not intervened;the cells in the LPS group were intervened with 1 mg·L-1 LPS;and the cells in the low-dose propofol group,medium-dose propofol group and high-dose propofol group were treated with 1 mg·L-1 LPS for 24 hours,then treated with 12.5,25.0 and 50.0 μmol·L-1 propofol,respectively.The expression levels of inflammatory factors interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in cell culture medium in each group were detected by enzyme-linked immunosorbent assay;the cell viability in each group was measured by cell counting kit-8;the cell proliferation in each group was detected by 5-ethynyl-2 ′-deoxyuridine method;the cell apoptosis in each group was detected by Hoechst 33258 staining;the number of adherent cells in each group was determined by cell adhesion assay;the invasion ability in each group was determined by Transwell chamber;the expression levels of Cyclin D1,caspase-3,E-cadherin,N-cadherin,Vimentin and fibronectin (FN) in each group were detected by Western blot.
Results　The IL-1β level,TNF-α level,cell viability,cell proliferation rate,number of adherent cells,number of invasive cells,and the levels of Cyclin D1,N-cadherin,Vimentin and FN protein in the LPS group were significantly higher than those in the control group(P<0.05);and the cell apoptosis rate,caspase-3 and E-cadherin level were significantly lower than those in the control group (P<0.05).The TNF-α level,cell viability,proliferation rate,number of adherent cells,number of invasive cells and the levels of Cyclin D1,N-cadherin,and Vimentin in the medium-dose propofol group and high-dose propofol group were significantly lower than those in the control group (P<0.05);while the cell apoptosis rate,the levels of caspase-3 and E-cadherin were significantly higher than those in the control group (P<0.05);there was no significant difference in the level of IL-1β between the medium-dose propofol group,high-dose propofol group and the control group (P>0.05);the level of FN in the high-dose propofol group was significantly lower than that in the control group (P<0.05),while there was no significant difference in the level of FN between the medium-dose propofol group and the control group (P>0.05).The number of invasive cells and the level of E-cadherin in the low-dose propofol group were significantly lower than those in the control group,while the level of Cyclin D1 was significantly higher than that in the control group (P<0.05);there was no significant difference in cell viability,cell proliferation rate,cell apoptosis rate,and number of adhesion cells between the low-dose propofol group and the control group (P>0.05).The IL-1β level and TNF-α level,cell viability,cell proliferation rate,number of adherent cells,number of invasive cells and the levels of Cyclin D1,N-cadherin,Vimentin and FN in the medium-dose propofol group and high-dose propofol group were significantly lower than those in the LPS group and low-dose propofol group(P<0.05);and the cell apoptosis rate,caspase-3 and E-cadherin levels were significantly higher than those in the LPS group and low-dose propofol group (P<0.05).The TNF-α level,number of adherent cells,number of invasive cells and the levels of N-cadherin and FN in the high-dose propofol group were significantly lower than those in the medium-dose propofol group (P<0.05);the cell apoptosis rate and E-cadherin level were significantly higher than those in the medium-dose propofol group (P<0.05).There was no statistically significant difference in the cell viability,cell proliferation rate,the levels of IL-1β,Cyclin D1,caspase-3 and Vimentin between the high-dose propofol group and medium-dose propofol group(P>0.05).The cell viability,cell proliferation rate,number of adherent cells,number of invasive cells,the levels of Cyclin D1,N-cadherin,Vimentin and FN in the low-dose propofol group were significantly lower than those in the LPS group(P<0.05);and the apoptosis rate and the levels of caspase-3 and E-cadherin were significantly higher than those in the LPS group (P<0.05);there was no significant difference in the levels of IL-1β and TNF-α between the low-dose propofol group and LPS group (P>0.05).
Conclusion　Propofol can relieve the LPS-induced inflammatory response,inhibit cell proliferation,adhesion,invasion,and induce apoptosis of hepatocellular carcinoma cells by inhibiting the epithelial-mesenchymal transition process.

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更新日期/Last Update: 2023-08-05