文章摘要
齐少霞,杨栋宝,靳涛,等.丙泊酚对脂多糖诱导的 MHCC97H细胞黏附、迁移、侵袭和炎症因子的影响及与核转录因子 -κB信号通路的关系[J].安徽医药,2025,29(2):263-267.
丙泊酚对脂多糖诱导的 MHCC97H细胞黏附、迁移、侵袭和炎症因子的影响及与核转录因子 -κB信号通路的关系
Effect of propofol on lipopolysaccharide-induced adhesion, migration, invasion and inflammatory factors of MHCC97H cells and its relationship with NF-κB signaling pathway
  
DOI:10.3969/j.issn.1009-6469.2025.02.010
中文关键词: 二异丙酚  MHCC97H  核转录因子 -κB信号通路  黏附  迁移  侵袭
英文关键词: Propofol  MHCC97H  Nuclear transcription factor-κB signaling pathway  Adhesion  Migration  Invasion
基金项目:河北省医学科学研究课题计划( 20220692)
作者单位
齐少霞 河北省沧州中西医结合医院麻醉一科河北沧州 061000 
杨栋宝 河北省沧州中西医结合医院麻醉一科河北沧州 061000 
靳涛 河北省沧州中西医结合医院麻醉一科河北沧州 061000 
王建华 河北省沧州中西医结合医院麻醉一科河北沧州 061000 
兰基山 河北省沧州中西医结合医院麻醉一科河北沧州 061000 
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中文摘要:
      目的探究丙泊酚与脂多糖( LPS)刺激下 MHCC97H细胞功能、炎症水平及核转录因子 -κB(NF-κB)表达的关联。方法该研究起止时间为 2021年 12月至 2022年 12月。体外培养人 MHCC97H细胞系,分为对照组(等量的溶剂),LPS组( 1 mg/ L LPS)实验组( LPS+6.25组、 LPS+12.5组、 LPS+25组, LPS组基础上分别加入 6.25、12.5和 25 μmol/L丙泊酚)用酶联免疫吸附试验、细胞,计数试剂盒检测炎症因子白细胞介素 6(IL-6)的表达水平和细胞活力筛选出丙泊酚的最适浓度进行,后续实验,后将细胞分为对照组、 LPS组、 LPS+25组和 LPS+25+抑制剂组( LPS+25组基础上联合 10 μmol/L BAY 11-7082)干预 24 h。细胞黏附实验测定黏附细胞数; Transwell小室法检测细胞迁移与侵袭水平;蛋白质印迹法测定上皮间质转化( EMT),及 NF-κB通路相关蛋白表达水平。结果根据细胞活力和炎症因子 IL-6表达选择 LPS+25组进行后续实验,与对照组相比, LPS组细胞黏附数、迁移数、侵袭数、 N-钙黏蛋白(N-cadherin)波形蛋白( Vimentin)、纤连蛋白( FN)、IκB激酶 α(IKKα)和 p-NF-κB p65蛋白水平分别为( 152.00±9.01)个、(84.01±10.44)个、(65.、67±3.06)个、 0.46±0.02、0.47±0.03、0.99±0.02、1.03±0.02、0.95±0.05上调, E-钙黏蛋白( E-cadherin)表达 0.42±0.02下调( P<0.05);与 LPS组相比, LPS+25组显著扭转了上述指标的变化( P<0.05);与 LPS+25组相比, LPS+25+抑制剂组加入 NF-κB通路抑制剂后,上述指标变化扭转得更为显著( P<0.05)。结论丙泊酚对 LPS刺激下 MHCC97H细胞炎症因子表达、黏附、迁移、侵袭能力及 EMT进程具有抑制作用,可能与 NF-κB通路活性受到抑制有关。
英文摘要:
      Objective To investigate the relationship between propofol and lipopolysaccharide (LPS) -induced MHCC97H cell func-tion, inflammation level and nuclear factor-κB (NF-κB) expression.Methods The study period was from December 2021 to December2022. Human MHCC97H cell lines were cultured in vitro and assigned into control group (equal volume of solvent), LPS group (1 mg/LLPS), experimental group (LPS+6.25 group, LPS+12.5 group, LPS+25 group, with 6.25, 12.5 and 25 μmol/L propofol added to LPSgroup, respectively). Enzyme-linked immunosorbent assay and cell counting kit were used to detect the expression level of inflammatory factor interleukin-6 (IL-6) and cell activity to screen out the optimal concentration of propofol for follow-up experiments. Then the cellswere assigned into control group, LPS group, LPS+25 group and LPS+25+inhibitor group (LPS+25 group was combined with 10 μmol/LBAY 11-7082), which were treated for 24 h. The number of adherent cells was measured by cell adhesion assay, cell migration and in-vasion were detected by Transwell chamber assay, and epithelial-mesenchymal transition (EMT) and NF-κB pathway-related proteins expression levels were determined by Western blotting.Results According to cell viability and the expression of inflammatory factor IL-6, LPS+25 group was selected for subsequent experiments. The counts of cell adhesion, migration, invasion, and N-cadherin, Vimen-tin, fibronectin (FN), IκB kinase α (IKKα) and p-NF-κB p65 protein expression levels [(152.00±9.01) cells, (84.01±10.44) cells,(65.67±3.06) cells, 0.46±0.02,0.47±0.03,0.99±0.02,1.03±0.02 and 0.95±0.05,respectively] in the LPS group were higher than those inthe control group, while E-cadherin expression level (0.42±0.02) was lower than that in the control group (P<0.05). The LPS+25 group significantly reversed the changes of the above indicators in comparison with LPS group (P<0.05). LPS+25+ inhibitor group reversed the changes of the above indicators after adding the NF-κB pathway inhibitor in comparison with LPS+25 group (P<0.05).Conclusion Propofol can inhibit the expression, adhesion, migration, invasion and EMT process of MHCC97H cells stimulated by LPS, which maybe related to the inhibition of NF-κB pathway activity.
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