Zhonghua nan ke xue = National journal of andrology · 2024
[Mechanism of icariin inhibiting the proliferation of human prostate cancer PC-3 cells: An exploration based on cell metabolomics].
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Wang Tao, Wang Wei, Xiong Wen-Jun, Zhang Zi-Jing, Wang Fei, Peng Yao-Hui, Chen Yan, Zeng Hai-Ping, Luo Li-Jie
Аннотация
OBJECTIVE: To study the mechanism of icariin inhibiting the proliferation of human PCa PC-3 cells based on cell metabolomics technology.
METHODS: We determined the proliferation activity of human PC-3 cells by methyl thiazolyl tetrazolium(MTT) assay, and compared the proliferation of the PC-3 cells among the control, 5-fluorouracil and icariin intervention groups. Using the Bligh Dyer method, we extracted endogenous metabolites from the cells, analyzed the metabolic profile by ultra-high pressure liquid chromatography tandem quadrupole time-of-flight mass spectrometry, identified the differential metabolites by principal component analysis and orthogonal partial least-squares discrimination analysis, and enriched the metabolic pathways based on the MetaboAnalyst database.
RESULTS: Icariin significantly inhibited the proliferation of human PCa PC-3 cells. A total of 89 differential metabolites were identified, mainly including amino acids, phosphatidylcholine, phosphatidylethanolamine, lysophosphatidylcholine, and lysophosphatidylethanolamine, all with the tendency to return to the normal level after icariin intervention. Icariin significantly downregulated the metabolic levels of the glycerophospholipid metabolites phosphatidylcholine, phosphatidylethanolamine, lysophosphatidylcholine and lysophosphatidylethanolamine, and upregulated those of amino acid metabolites tryptophan, leucine, and proline in the PC-3 cells.
CONCLUSION: Icariin inhibits the proliferation of human PCa PC-3 cells, which may be closely related to its regulatory effect on lipid metabolism (glycerophospholipid metabolism) and amino acid metabolism.
METHODS: We determined the proliferation activity of human PC-3 cells by methyl thiazolyl tetrazolium(MTT) assay, and compared the proliferation of the PC-3 cells among the control, 5-fluorouracil and icariin intervention groups. Using the Bligh Dyer method, we extracted endogenous metabolites from the cells, analyzed the metabolic profile by ultra-high pressure liquid chromatography tandem quadrupole time-of-flight mass spectrometry, identified the differential metabolites by principal component analysis and orthogonal partial least-squares discrimination analysis, and enriched the metabolic pathways based on the MetaboAnalyst database.
RESULTS: Icariin significantly inhibited the proliferation of human PCa PC-3 cells. A total of 89 differential metabolites were identified, mainly including amino acids, phosphatidylcholine, phosphatidylethanolamine, lysophosphatidylcholine, and lysophosphatidylethanolamine, all with the tendency to return to the normal level after icariin intervention. Icariin significantly downregulated the metabolic levels of the glycerophospholipid metabolites phosphatidylcholine, phosphatidylethanolamine, lysophosphatidylcholine and lysophosphatidylethanolamine, and upregulated those of amino acid metabolites tryptophan, leucine, and proline in the PC-3 cells.
CONCLUSION: Icariin inhibits the proliferation of human PCa PC-3 cells, which may be closely related to its regulatory effect on lipid metabolism (glycerophospholipid metabolism) and amino acid metabolism.