| 龙云,张范.山慈菇-红大戟药对通过PI3K/Akt/Bad信号通路调控A549细胞增殖、迁移及凋亡[J].安徽医药,待发表. |
| 山慈菇-红大戟药对通过PI3K/Akt/Bad信号通路调控A549细胞增殖、迁移及凋亡 |
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| 投稿时间：2025-03-03 录用日期：2025-04-18 |
| DOI： |
| 中文关键词: 山慈菇 红大戟 药对 A549细胞 PI3K/Akt/Bad信号通路 增殖 迁移 凋亡 |
| 英文关键词: |
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| 中文摘要: |
| 目的：探讨山慈菇-红大戟药对通过调控PI3K/Akt/Bad信号通路对A549细胞增殖、迁移、凋亡的影响。方法：通过CCK-8法筛选出最佳的药对配伍，利用划痕愈合、细胞凋亡、线粒体膜电位、活性氧测定等实验证明最佳的药对配伍在A549细胞增殖中的抑制作用和促进凋亡的作用，再通过蛋白免疫印迹实验检测PI3K/Akt/Bad信号通路相关蛋白表达情况。结果：山慈菇-红大戟2∶1组（10、20、40、80、160、320 μg/mL）能显著降低A549细胞活力（P＜0.05），为最佳药对配伍；与对照组相比，山慈菇-红大戟2∶1组（40、80、160、320 μg/mL）细胞增殖、迁移能力显著降低（P＜0.05）；与对照组相比，山慈菇-红大戟2∶1组（10、20、40、80、160、320 μg/mL）线粒体膜电位水平显著降低（P＜0.05），（20、40、80、160、320 μg/mL）活性氧水平、凋亡率显著升高（P＜0.05），；与对照组相比，山慈菇-红大戟2∶1组（80、160、320 μg/mL）p-PI3K/PI3K、p-Akt/Akt、Bcl2的表达明显下调，Bax的表达显著上调（P＜0.05），而（320 μg/mL）Bad、Bax的表达则显著上调（P＜0.05）。结论：山慈菇-红大戟药对2∶1可能通过调控PI3K/Akt/Bad信号通路抑制A549细胞的增殖和迁移，促进A549细胞的凋亡。 |
| 英文摘要: |
| Abstract：Objective To investigate the effects of the Shancigu-Hongdaji pairing on the proliferation, migration and apoptosis of A549 cells through the modulation of the PI3K/Akt/Bad signaling pathway. Methods The optimal pairing of drugs was screened by CCK-8 assay, and the proliferation inhibition and pro-apoptotic effects of the optimal pairing of drugs on A549 cells were demonstrated by scratch healing, apoptosis, mitochondrial membrane potential, and reactive oxygen species assay, and then the expression of proteins related to the PI3K/Akt/Bad signaling pathway was detected by protein immunoblotting assay. Results The Shancigu-Hongdaji 2:1 group (10, 20, 40, 80, 160, 320 μg/mL) could significantly reduced the viability of A549 cells (P<0.05), which was the optimal pairing of drugs; compared with the control group, the Shancigu-Hongdaji 2:1 group (40, 80, 160, 320 μg/mL) had significantly reduced the ability of cell proliferation and migration (P<0.05); the mitochondrial membrane potential levels were significantly lower (P<0.05) in the Shancigu-Hongdaji 2:1 group (10, 20, 40, 80, 160, 320 μg/mL), and the reactive oxygen species levels and apoptosis rates were significantly higher (P<0.05) in the Shancigu-Hongdaji 2:1 group(20, 40, 80, 160, 320 μg/mL); the expression of p-PI3K, p-Akt, and Bcl2 was significantly down-regulated and the expression of Bax was significantly up-regulated (P<0.05) in the Shancigu-Hongdaji 2:1 group (80, 160, 320 μg/mL), whereas the expression of (320 μg/mL)Bad was significantly up-regulated (P<0.05) in the Shancigu-Hongdaji 2:1 group. Conclusion Shancigu-Hongdaji 2:1 may inhibit the proliferation and migration of A549 cells and promote the apoptosis of A549 cells by regulating the PI3K/Akt/Bad signaling pathway. |
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