刘炯,汪向飞,江斌.利多卡因对胰腺癌细胞PANC-1增殖、凋亡和STING/IRF3/IFN-β通路的影响.[J].中南医学科学杂志.,2022,(4):499-503. |
利多卡因对胰腺癌细胞PANC-1增殖、凋亡和STING/IRF3/IFN-β通路的影响 |
Effects of lidocaine on proliferation, apoptosis and STING/IRF3/IFN-β pathway of pancreatic cancer cell PANC-1 |
投稿时间:2021-05-11 修订日期:2021-11-13 |
DOI:10.15972/j.cnki.43-1509/r.2022.04.008 |
中文关键词: 利多卡因 STING/IRF3/IFN-β通路 胰腺癌 细胞增殖 细胞凋亡 |
英文关键词:lidocaine STING/IRF3/IFN-β pathway pancreatic cancer cell proliferation cell apoptosis |
基金项目:湖北省陈孝平科技发展基金项目(CXPJJH11800001-2018246) 作者简介:刘炯,硕士,主治医师,研究方向为肝癌、胰腺癌诊治及病理生理研究,E-mail为w1017y1926@126.com。通信作者江斌,博士,主任医师,研究方向为胆道疾病的诊治及病理生理研究,E-mail为jiangbin5799@163.com。 |
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中文摘要: |
目的探讨利多卡因对胰腺癌细胞PANC-1增殖、凋亡和干扰素基因刺激因子(STING)/干扰素调节因子3(IRF3)/干扰素-β(IFN-β)通路的影响。 方法体外培养PANC-1细胞,阴性对照组不干预,利多卡因低、中、高剂量组分别用20、40、80 mg/L利多卡因干预,阳性对照组用10 mg/L吉西他滨干预。采用CCK-8和流式细胞术检测细胞增殖率和凋亡率,酶标仪检测细胞肿瘤坏死因子-α(TNF-α)和IFN-β水平,荧光定量聚合酶链反应和蛋白印迹法检测细胞STING、IRF3、Akt和Caspase-3 mRNA及蛋白水平。 结果与阴性对照组比较,利多卡因低、中、高剂量组及阳性对照组细胞增殖率、TNF-α水平、Akt mRNA和蛋白水平降低,细胞凋亡率、IFN-β水平及STING、IRF3、Caspase-3 mRNA和蛋白水平增加;利多卡因组随利多卡因剂量增加呈剂量效应关系,但利多卡因组效应未及阳性对照组(P<0.05)。 结论利多卡因抑制PANC-1细胞增殖,促进PANC-1细胞凋亡,其机制可能与STING/IRF3/IFN-β通路的激活有关。 |
英文摘要: |
To investigate the effect of lidocaine on proliferation, apoptosis and stimulator of interferon genes(STING)/interferon regulatory factor-3 (IRF3)/interferon-β (IFN-β) pathway of pancreatic cancer cell PANC-1. MethodsPANC-1 cells were cultured in vitro, and the negative control group was not intervened, the lidocaine low-dose, middle-dose and high-dose groups were intervened with 20,40, and 80 mg/L lidocaine, respectively, and the positive control group was intervened with 10 mg/L gemcitabine. Cell proliferation rate and apoptosis rate were detected by CCK-8 and flow cytometry. Microplate reader was used to detect the levels of tumor necrosis factor-α (TNF-α) and IFN-β, and the mRNA and protein levels of STING, IRF3, Akt and Caspase-3 were detected by fluorescence quantitative polymerase chain reaction and western blotting. ResultsCompared with the negative control group, the cell proliferation rate, TNF-α, Akt mRNA and protein levels of the lidocaine low, medium and high dose groups and the positive control group decreased, and the apoptosis rate, IFN-β, STING, IRF3 and Caspase-3 mRNA and protein levels increased, and as the dose of lidocaine increased, the effects of each dose group of lidocaine showed a dose-response relationship, but the effect was not as good as that of the positive control group(P<0.05). ConclusionLidocaine can inhibit the proliferation of PANC-1 cells and promote the apoptosis of PANC-1 cells. The mechanism may be related to the activation of the STING/IRF3/IFN-β pathway by lidocaine. |
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