针对磷脂酰肌醇3-激酶/AKT1信号通路:梧桐树提取物诱导肺腺癌细胞凋亡

IF 0.9 4区 材料科学
Xiaodong Song, Shanshan Guo, Mei Wang, Rui Fan, Yang Li, Qiquan Yu, Qiuli Bao, Chunxiao Wu, Ze-Quan Zhang, Kaiyao Zhang
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引用次数: 0

摘要

本研究旨在通过PI3K/AKT1信号通路研究益普氏提取物对肺腺癌A549细胞的抑制作用。研究人员用不同浓度的Iphigenia indica提取物处理A549细胞,并进行了各种测定。结果表明,随着党参提取物浓度的增加,A549细胞的活力降低。与对照组相比,党参提取物和PI3K/AKT抑制剂对A549细胞的增殖和集落形成具有更高的抑制率,减少了迁移和侵袭,并诱导了细胞凋亡。此外,Iphigenia indica提取物和PI3K/AKT抑制剂降低了Bcl-2、PI3K和AKT1的蛋白水平,并增加了Bax的水平。研究结果表明,党参提取物可能通过PI3K/AKT1信号通路,通过诱导细胞凋亡、抑制增殖、迁移和侵袭,以及调节Bcl-2、Bax、PI3K和AKT1的表达,抑制肺腺癌细胞的恶性生物学行为。总的来说,益母草提取物可能具有治疗肺腺癌的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Targeting the Phosphatidylinositol 3-Kinase/AKT1 Signaling Pathway: Iphigenia indica Extracts Induce Apoptosis in Lung Adenocarcinoma Cells
This study aimed to investigate the inhibitory effects of Iphigenia indica extracts on lung adenocarcinoma A549 cells through the PI3K/AKT1 signaling pathway. The researchers treated A549 cells with different concentrations of Iphigenia indica extracts and conducted various assays. The results showed that the viability of A549 cells decreased with increasing concentration of Iphigenia indica extracts. Iphigenia indica extracts and PI3K/AKT inhibitor had a higher inhibitory rate of cell proliferation and colony formation, reduced migration and invasion, and induced apoptosis in A549 cells compared to the control group. Furthermore, Iphigenia indica extracts and PI3K/AKT inhibitor reduced the protein levels of Bcl-2, PI3K, and AKT1 and increased the level of Bax. The findings suggest that Iphigenia indica extracts may inhibit malignant biological behaviors of lung adenocarcinoma cells through the PI3K/AKT1 signaling pathway by inducing apoptosis, inhibiting proliferation, migration and invasion, and regulating the expression of Bcl-2, Bax, PI3K, and AKT1. Overall, Iphigenia indica extracts may have potential as a therapeutic agent for lung adenocarcinoma.
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来源期刊
Science of Advanced Materials
Science of Advanced Materials NANOSCIENCE & NANOTECHNOLOGY-MATERIALS SCIENCE, MULTIDISCIPLINARY
自引率
11.10%
发文量
98
审稿时长
4.4 months
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