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[15]
          转移来实现 。但 FAK/MEK/ERK 信号通路在 LC 中的                        外基础与临床杂志,2020,27(2):168-172.
          作用还有待进一步研究。本研究结果显示,CSL处理后                               DONG B W,LI Z Y,LI W D,et al. Effects of disulfiram
          Huh7/Len细胞中p-FAK、p-MEK、p-ERK、Bcl-2蛋白相对                  combined with copper ions on proliferation and apoptosis
          表达量均显著降低,Bax、caspase-3蛋白相对表达量均显                         of lenvatinib resistance Huh7 cells[J]. Chin J Bases Clin
          著升高,这提示CSL可能通过抑制FAK/MEK/ERK信号                           Gen Surg,2020,27(2):168-172.
                                                             [ 7 ]  孙懿,宋莹莹,张聪,等. 雷公藤红素激活AMPK信号通
          通路,促进凋亡相关因子 caspase-3、Bax 介导的细胞凋
                                                                  路抑制肝癌 HepG2 细胞增殖的作用研究[J]. 中国药师,
          亡,从而抑制 LC 的进展。此外,本研究还发现,与 CSL
                                                                  2021,24(11):1961-1966,1982.
          高浓度组比较,FAK 激活剂 Zn27 联合高浓度 CSL 处理
                                                                  SUN Y,SONG Y Y,ZHANG C,et al. Effects and mecha‐
          后细胞中p-FAK、p-MEK、p-ERK、Bcl-2蛋白相对表达量
                                                                  nism of celastrol on the proliferation of hepatocellular car‐
          均显著升高,细胞凋亡率、ROS 水平以及 Bax、caspase-3                      cinoma HepG2 cells by activating AMPK signal pathway
          蛋白相对表达量均显著降低,可见 Zn27 可逆转 CSL 的                          [J]. China Pharm,2021,24(11):1961-1966,1982.
          抗 LC 作用,这进一步说明 CSL 通过抑制 FAK/MEK/                   [ 8 ]  RASHMI,MORE S K,WANG Q G,et al. ZINC40099027
          ERK 信号通路来提高化疗耐药性,抑制细胞存活和扩                               activates human focal adhesion kinase by accelerating the
          散,加速细胞凋亡。                                               enzymatic activity of the FAK kinase domain[J]. Pharma‐
              综上所述,CSL能增强氧化应激,促进细胞凋亡,抑                            col Res Perspect,2021,9(2):e00737.
          制 LC 细胞恶性进展和化疗耐药性,其机制可能与抑制                         [ 9 ]  POPE E D 3rd,KIMBROUGH E O,VEMIREDDY L P,
          FAK/MEK/ERK 信号通路有关。上述结论可能为 LC 发                         et al. Aberrant lipid metabolism as a therapeutic target in
          展的潜在机制提供新的见解,有利于临床推广应用。但                                liver cancer[J]. Expert Opin Ther Targets,2019,23(6):
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          本研究未探讨激活剂对其的干扰,且缺乏体内实验验
                                                             [10]  LUO P,LIU D D,ZHANG Q,et al. Celastrol induces fer‐
          证,后续将进一步研究以确认结论。
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          中国药房  2024年第35卷第20期                                              China Pharmacy  2024 Vol. 35  No. 20    · 2481 ·
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