| 王欣玉,裴晓东,何志龙,等.尾叶香茶菜丙素对肝癌耐药株 HepG2/ADM细胞体外活性的影响[J].安徽医药,2021,25(11):2131-2135. |
| 尾叶香茶菜丙素对肝癌耐药株 HepG2/ADM细胞体外活性的影响 |
| In vitro activity of Kamebakaurin on hepatocellular carcinoma resistant strain HepG2/ADM cells |
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| DOI：10.3969/j.issn.1009-6469.2021.11.003 |
| 中文关键词: 香茶菜属 肝肿瘤 抗药性，肿瘤 尾叶香茶菜丙素 PENT-AKT通路 凋亡 迁移 |
| 英文关键词: Plectranthus Liver neoplasms Drug resistance,neoplasm Kamebakaurin PTEN-AKT pathway Apoptosis Migration |
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| 中文摘要: |
| 目的探究尾叶香茶菜丙素( Kamebakaurin)对 HepG2/ADM(肝癌细胞耐阿霉素耐药株)细胞体外活性。方法通过 2-(2-甲氧基 -4-硝基苯基) -3-(4-硝基苯基) -5-(2，4-二磺酸苯) -2H-四唑单钠盐( CCK-8法)测定尾叶香茶菜丙素和阿霉素(ADM)对 HepG2/ADM细胞的生长活力抑制率；通过流式细胞术测定尾叶香茶菜丙素对细胞周期和细胞凋亡的影响；运用 Transwell小室实验和划痕愈合实验检验尾叶香茶菜丙素对 HepG2/ADM细胞迁移能力影响，用实时荧光定量 PCR检测耐药相关基因表达，通过蛋白印迹法( Western blotting)分析 PTEN-AKT信号通路。结果尾叶香茶菜丙素对 HepG2/ADM细胞的 IC50值为 62.96 μmol/L，ADM在 1 mg/mL(184 μmol/L)只有 26.5%抑制率，说明 HepG2/ADM细胞耐药株对尾叶香茶菜丙素敏感度高于阿霉素；尾叶香茶菜丙素诱导肝癌细胞 HepG2/ADM细胞的凋亡，阻滞细胞在 G2期，且呈浓度依赖性；尾叶香茶菜丙素具有抑制 HepG2/ADM细胞穿过小室的能力和平板愈合能力，显示尾叶香茶菜丙素可抑制其迁移能力； Western blotting显示尾叶香茶菜丙素通过抑制 MDR1和 PENT-AKT通路发挥以上功能。结论尾叶香茶菜丙素抑制 MDR1蛋白表达从而逆转 HepG2/ADM细胞对药物的敏感性，通过抑制 PENT-AKT通路的激活从而促进 HepG2/ADM细胞的凋亡并抑制其迁移能力。 |
| 英文摘要: |
| Objective To investigate the activity of Kamebakaurin on HepG2/ADM cells in vitro.Methods CCK-8 kit was used to determine the cell viability of HepG2/ADM cells treated by Kamebakaurin and adriamycin (ADM). The effects of Kamebakaurin on cellcycle and apoptosis were determined by flow cytometry. Transwell assay and wound healing experiments were used to measure the migratory and invasive ability on HepG2/ADM cells, drug resistance related genes were detected by real-time quantitative PCR. PTENAKT pathway was assayed by western blotting.Results The IC50 value was 62.96 μmol/L of Kamebakaurin on HepG2/ADM cells,while 1 mg/mL ADM (184 μmol/L) on HepG2/ADM cells had an inhibition of 26.5%, therefore HepG2/ADM cells were more sensitiveto Kamebakaurin than ADM. We also found Kamebakaurin promoted the apoptosis of HepG2/ADM cells, arrested cell cycle in G2phase and showed concentration dependence. Moreover, Kamebakaurin inhibited the migratory ability of HepG2/ADM cells by suppressing the expression of MDR1 and PTEN-AKT pathway. Kamebakaurin inhibited the ability of HepG2/ADM cells to pass the transwell and to heal wound gap, indicating that Kamebakaurin could suppress its migration ability.Conclusion Kamebakaurin reverses the sensitivity to drug of HepG2/ADM cells by inhibiting MDR1 protein expression,promoting the apoptosis of HepG2/ADM cells andsuppressing its migration ability by inactivating PTEN-AKT pathway. |
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