Effect of fudosteine on lung cancer cells in an inflammatory microenvironment based on metabolomics
10.16438/j.0513-4870.2021-1094
- VernacularTitle:福多司坦干预炎症微环境下肺癌细胞的代谢组学研究
- Author:
Yi-fei WANG
1
;
Qi-le ZHANG
1
;
Xin LI
1
;
Meng-ting GAO
1
;
Li ZHANG
1
;
An-wei DING
1
;
Wen-yu XIA
2
;
Wei-feng YAO
1
Author Information
1. Jiangsu Key Laboratory for High Technology Research of TCM Formulae and Jiangsu Collaborative Innovation Center of Chinese Medicinal Resources Industrialization, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China
2. Jiangsu Chia Tai Fenghai Pharmaceutical Co., Ltd., Yancheng 224100, China
- Publication Type:Research Article
- Keywords:
fudosteine;
inflammatory microenvironment;
A549;
metabolomics;
GC-MS
- From:
Acta Pharmaceutica Sinica
2022;57(2):419-427
- CountryChina
- Language:Chinese
-
Abstract:
GC-MS metabolomics was used to investigate the effects of fudosteine on lung cancer A549 cells in an inflammatory microenvironment. Eleven metabolites (malic acid, isoleucine, lactose, galactinol, creatinine, gluconic acid, oleic acid, phosphate, S-carboxymethyl-L-cysteine, uridine and tagatose) were identified in the metabolomics results and could be used as biomarkers of fudosteine treatment. Pathway enrichment analysis showed that the metabolic pathways of amino acids including isoleucine, valine, leucine, glycine, serine and threonine were significantly altered, as were the metabolic pathways of carbohydrates such as galactose and pentose phosphate. Fudosteine significantly reduced the level of inflammatory factors in A549 cells and corrected the inflammatory microenvironment by interfering with the effects of amino acid metabolites and amino acid metabolism pathways. This study reveals that fudosteine may be able to inhibit the continuous inflammatory response and prevent the further progression of lung cancer by suppressing the inflammatory microenvironment.
