| 引用本文:孙平一1，刘娟2，刘思远2，王荣1，郑心3.阳和汤加味对肺腺癌细胞的影响及作用机制[J].世界中医药,2024,(24):. |
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| 阳和汤加味对肺腺癌细胞的影响及作用机制 |
| Effect and Mechanism of Modified Yanghe Decoction on Lung Adenocarcinoma Cells |
| 投稿时间：2024-01-14 |
| DOI：10.3969/j.issn.1673-7202.2024.24.005 |
| 中文关键词: 阳和汤加味 经典名方 肺腺癌 药理作用 作用机制 miR-1-3p 磷脂酰肌醇3-激酶/蛋白激酶B/哺乳动物雷帕霉素靶蛋白（PI3K/AKT/mTOR） 合理运用 |
| English Keywords:Modified Yanghe Decoction Classic prescription Lung adenocarcinoma Pharmacological action Mechanism MiR-1-3p PI3K/AKT/mTOR Reasonable application |
| 基金项目:国家自然科学基金项目（82374288）；山东省自然科学基金项目（ZR2021MH274）；青岛市科技惠民示范专项（23-2-8-smjk-4-nsh） |
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| 中文摘要: |
| 目的：观察阳和汤加味含药血清对人肺腺癌细胞（A549、H1975）及其miR-1-3p/磷脂酰肌醇3-激酶/蛋白激酶B/哺乳动物雷帕霉素靶蛋白(PI3K/AKT/mTOR)信号通路的影响。方法：构建A549、H1975细胞微小RNA-1-3p（miR-1-3p）过表达及干扰稳转株，给予阳和汤加味含药血清干预，通过肺腺癌细胞增殖及毒性检测实验（CCK-8）、划痕、Transwell实验检测细胞增殖、迁移及侵袭能力；实时定量聚合酶链式反应（RT-qPCR）检测miR-1-3p mRNA表达水平；蛋白质印迹法检测PI3K/AKT/mTOR通路蛋白表达水平。结果：miR-1-3p mRNA表达水平在2种肺腺癌细胞（A549、H1975）中明显低于正常肺泡上皮细胞Beas-2b（P<0.05）；与空白血清比较，含药血清组肺腺癌细胞的miR-1-3p表达量增加，细胞增殖、迁移及侵袭能力受到明显抑制，干扰miR-1-3p后逆转了这种抑制作用（P<0.05）；与空载组比较，miR-1-3p过表达组细胞磷脂酰肌醇3-激酶（PI3K）、蛋白激酶B（AKT）、哺乳动物雷帕霉素靶蛋白（mTOR）蛋白表达量下降（P<0.05）；含药血清干预后，2种肺腺癌细胞PI3K/AKT/mTOR信号通路蛋白表达量降低，干扰miR-1-3p可逆转对通路蛋白表达水平的抑制作用（P<0.05）。结论：阳和汤加味含药血清能够抑制肺腺癌细胞A549、H1975的增殖、迁移及侵袭，其作用机制可能与调控miR-1-3p的表达进而抑制PI3K/AKT/mTOR信号通路有关。 |
| English Summary: |
| To observe the effect of modified Yanghe Decoction(YHD)-medicated serum on human lung adenocarcinoma cells(A549，H1975) and its influence on the miR-1-3p/phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin(PI3K/AKT/mTOR) signaling pathway.Methods:A549 and H1975 cells were established as stable overexpression and interference cell lines of miR-1-3p.The cells were treated with modified YHD-medicated serum.The Cell Counting Kit-8(CCK-8)，scratch test，and Transwell assay were used to assess cell proliferation，migration，and invasion of lung adenocarcinoma cells.Real-time quantitative PCR(RT-qPCR) was used to measure miR-1-3p mRNA expression，and Western blot was used to detect the expression levels of proteins in the PI3K/AKT/mTOR pathway.Results:The expression level of miR-1-3p mRNA in A549 and H1975 lung adenocarcinoma cells was significantly lower than that in normal alveolar epithelial cells(Beas-2b)(P<0.05).Compared with the blank serum group，the drug-medicated serum group increased miR-1-3p expression and significantly inhibited cell proliferation，migration，and invasion.This inhibitory effect was reversed after miR-1-3p interference(P<0.05).Compared with the control group，the miR-1-3p overexpression group showed reduced expression of PI3K，AKT，and mTOR proteins(P<0.05).After treatment with drug-medicated serum，the protein expression levels of the PI3K/AKT/mTOR signaling pathway in both cell lines were reduced，and the inhibition of pathway protein expression was reversed by miR-1-3p interference(P<0.05).Conclusion:Modified YHD-medicated serum can inhibit the proliferation，migration，and invasion of lung adenocarcinoma cells(A549，H1975).The mechanism of action may involve the regulation of miR-1-3p expression，which subsequently inhibits the PI3K/AKT/mTOR signaling pathway. |
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