| 朱征全,王松,郭宏志,等.重楼皂苷 Ⅶ通过 p38丝裂原活化蛋白激酶信号通路对肝癌细胞恶性生物学行为的影响[J].安徽医药,2024,28(3):470-474. |
| 重楼皂苷 Ⅶ通过 p38丝裂原活化蛋白激酶信号通路对肝癌细胞恶性生物学行为的影响 |
| Effect of Polyphyllin Ⅶ on malignant biological behavior of hepatocellular carcinoma cells through p38 MAPK signaling pathway |
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| DOI：10.3969/j.issn.1009-6469.2024.03.009 |
| 中文关键词: 重楼 皂苷类 p38丝裂原活化蛋白激酶 肝癌 增殖 侵袭 迁移 |
| 英文关键词: Paris root Saponins p38 mitogen-activated protein kinase Liver cancer Proliferation Invasion Migration |
| 基金项目:河南省医学科技攻关计划(联合共建)项目( LHGJ20190640) |
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| 中文摘要: |
| 目的观察重楼皂苷 Ⅶ对肝癌细胞恶性生物学行为的影响，并探讨相关机制。方法于 2021年 6月至 2022年 6月，对数期人肝癌 HepG2细胞，分为对照组(常规培养)、重楼皂苷 Ⅶ组(重楼皂苷 Ⅶ 0.8 μmol/L)、SB203580［p38丝裂原活化蛋白激取酶( p38 MAPK)信号通路抑制剂］组( SB203580 10 μmol/L)、联合组(重楼皂苷 Ⅶ 0.8 μmol/L、SB203580 10 μmol/L)。噻唑蓝法检测细胞增殖能力；膜联蛋白 Ⅴ(Annexin Ⅴ)/碘化丙啶( PI)双染法检测细胞凋亡率；划痕实验检测细胞迁移能力；小室实验检测细胞侵袭能力；蛋白质印迹法检测细胞 p38 MAPK、磷酸化 p38丝裂原活化蛋白激酶( p-p38 MAPK)、细胞外信号调节激酶(ERK)1/2、磷酸化细胞外信号调节激酶( p-ERK1/2)蛋白表达。结果与对照组 24、48、72 h吸光度值，迁移率( 74.33±9.37)%，凋亡率( 3.25±0.78)%，p-p38 MAPK/p38 MAPK、p-ERK1/2/ERK1/2及侵袭细胞数( 364.92±47.99)个比较，重楼皂苷 Ⅶ组 24、48、 72 h吸光度值，迁移率( 11.21±3.35)%降低，凋亡率( 39.87±8.94)%，p-p38 MAPK/p38 MAPK、p-ERK1/2/ERK1/2升高，侵袭细胞数( 54.84±7.41)个减少( P<0.05)； SB203580组 24、48、72 h吸光度值，迁移率( 89.30±14.56)%升高，凋亡率( 1.05±0.15)%，p-p38 MAPK/p38 MAPK、p-ERK1/2/ERK1/2降低，侵袭细胞数( 617.04±75.34)个增加( P<0.05)。与重楼皂苷 Ⅶ组比较，联合组 24、48、 72 h吸光度值，迁移率( 40.52±8.18)%升高，凋亡率( 11.30±2.80)%，p-p38 MAPK/p38 MAPK、p-ERK1/2/ERK1/2降低，侵袭细胞数( 141.36±16.75)个增加( P<0.05)；与 SB203580组比较，联合组 24、48、72 h吸光度值、迁移率降低，凋亡率、 p-p38 MAPK/p38 MAPK、p-ERK1/2/ERK1/2升高，侵袭细胞数减少( P<0.05)。结论重楼皂苷 Ⅶ可抑制肝癌 HepG2细胞增殖、迁移及侵袭等恶性生物学行为，并诱导其凋亡，作用机制可能与激活 p38 MAPK信号通路相关。 |
| 英文摘要: |
| Objective To observe the effect of Polyphyllin Ⅶ on the malignant biological behavior of hepatoma cells, and to explore the related mechanism.Methods From June 2021 to June 2022, HepG2 cells in logarithmic phase were assigned into control group(conventional culture), Polyphyllin Ⅶ group (Polyphyllin Ⅶ 0.8 μmol/L), SB203580 [p38 mitogen-activated protein kinase (p38MAPK) signaling pathway Inhibitor] group (SB203580 10 μmol/L), combined group (Polyphyllin Ⅶ 0.8 μmol/L, SB203580 10 μmol/L). Cell proliferation was detected by methylthiazolyldiphenyl-tetrazolium bromide assay. The apoptosis rate of cells was detected byAnnexin Ⅴ/propidine iodide (PI) double staining. The scratch assay was used to examine cell migration ability. The cell invasive abilitywas detected by a small laboratory experiment. Western blotting was used to detect the protein expressions of p38 MAPK, phosphorylat.ed p38 mitogen-activated protein kinase (p-p38 MAPK), extracellular signal-regulated kinase (ERK) 1/2 and phosphorylated extracellu. lar signal-regulated kinase (p-ERK1/2).Results Compared with the absorbance value at 24 h, 48 h and 72 h, the mobility (74.33± 9.37)%, the apoptosis rate (3.25±0.78)%, p-p38 MAPK/p38 MAPK, p-ERK1/2/ERK1/2, and the number of membrane-penetrating cells[(364.92±47.99) cells] in the control group, the absorbance value at 24, 48, and 72 h, migration rate (11.21±3.35)%, and the number ofmembranous cells [(54.84±7.41) cells] were decreased, apoptosis rate (39.87±8.94)% , p-p38 MAPK/p38 MAPK, p-ERK1/2/ERK1/2 were increased in the Polyphyllin Ⅶ group (P<0.05); the absorbance value at 24, 48, and 72 h, migration rate (89.30±14.56)% and thenumber of membranous cells [(617.04±75.34) cells] were increased, apoptosis rate (1.05±0.15)%, p-p38 MAPK/p38 MAPK, p-ERK1/2/ ERK1/2 were decreased in the SB203580 group (P<0.05). Compared with the Polyphyllin Ⅶ group, the absorbance value at 24, 48, and72 h, migration rate (40.52±8.18)% and the number of membranous cells [(141.36±16.75) cells] were increased, apoptosis rate (11.30±2.80)% , p-p38 MAPK/p38 MAPK, p-ERK1/2/ERK1/2 were decreased in the combination group (P<0.05). Compared with theSB203580 group, the absorbance value at 24, 48, and 72 h, migration rate and the number of membranous cells were decreased, apopto.sis rate, p-p38 MAPK/p38 MAPK, p-ERK1/2/ERK1/2 were increased in the combination group (P<0.05).Conclusions Polyphyllin Ⅶcan inhibit the malignant biological behaviors such as proliferation, migration and invasion of liver cancer HepG2 cells, and inducetheir apoptosis. The mechanism may be related to the activation of p38 MAPK signaling pathway. |
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