DOI: 10.57760/sciencedb.nprd.00029
title: Data set of total alkaloids of Fritillariae Pallidiflorae Bulbus in the treatment of pulmonary fibrosis based on mass spectrometry analysis and network pharmacology
title: 基于质谱分析和网络药理学的伊贝母总生物碱治疗肺纤维化的数据集

description: To investigate the effective components and mechanisms of action of total alkaloids of Fritillariae Pallidiflorae Bulbus (FPB-TA) in inhibiting pulmonary fibrosis (PF). This study used HPLC-Q-TOF-MS/MS and LC-MS/MS techniques to analyze FPB-TA. Potential targets for the treatment of PF were screened using databases such as TCMSP. A protein-protein interaction network was constructed using the STRING database, and GO biofunctional annotation and KEGG pathway enrichment were performed on core targets. Molecular docking techniques were used to simulate the binding ability of alkaloid components in Fritillariae Pallidiflorae Bulbus to key targets. A transforming growth factor-beta 1 (TGF-β1)-induced PF in vitro model of A549 cells was constructed. Western blot and Sirius red staining were used to verify the therapeutic effect and mechanism of FPB-TA on PF. Mass spectrometry analysis identified 241 compounds in 24 classes, with nine alkaloids accounting for 55.362% of the total alkaloid content. Network pharmacology yielded 115 intersection targets, and protein-protein interaction analysis screened 22 targets with 181 interaction edges. KEGG enrichment involves the Ras-related protein 1 (RAP1) signaling pathway, cancer pathway, mitogen-activated protein kinase (MAPK) signaling pathway, etc. The RAP1 signaling pathway was selected for further study. Molecular docking was performed between the alkaloid components of the active ingredient and the key protein RAP1B in the RAP1 signaling pathway, showing good binding affinity between the active ingredient and the key protein. In vitro experiments showed that FPB-TA can effectively improve collagen deposition in TGF-β1-stimulated A549 cells and effectively inhibit RAP1B protein expression. This study revealed the chemical components of FPB-TA and explored its potential molecular mechanism for alleviating PF, providing a theoretical basis and research direction for further in-depth exploration of its mechanism of action.
description: To investigate the effective components and mechanisms of action of total alkaloids of Fritillariae Pallidiflorae Bulbus (FPB-TA) in inhibiting pulmonary fibrosis (PF). This study used HPLC-Q-TOF-MS/MS and LC-MS/MS techniques to analyze FPB-TA. Potential targets for the treatment of PF were screened using databases such as TCMSP. A protein-protein interaction network was constructed using the STRING database, and GO biofunctional annotation and KEGG pathway enrichment were performed on core targets. Molecular docking techniques were used to simulate the binding ability of alkaloid components in Fritillariae Pallidiflorae Bulbus to key targets. A transforming growth factor-beta 1 (TGF-β1)-induced PF in vitro model of A549 cells was constructed. Western blot and Sirius red staining were used to verify the therapeutic effect and mechanism of FPB-TA on PF. Mass spectrometry analysis identified 241 compounds in 24 classes, with nine alkaloids accounting for 55.362% of the total alkaloid content. Network pharmacology yielded 115 intersection targets, and protein-protein interaction analysis screened 22 targets with 181 interaction edges. KEGG enrichment involves the Ras-related protein 1 (RAP1) signaling pathway, cancer pathway, mitogen-activated protein kinase (MAPK) signaling pathway, etc. The RAP1 signaling pathway was selected for further study. Molecular docking was performed between the alkaloid components of the active ingredient and the key protein RAP1B in the RAP1 signaling pathway, showing good binding affinity between the active ingredient and the key protein. In vitro experiments showed that FPB-TA can effectively improve collagen deposition in TGF-β1-stimulated A549 cells and effectively inhibit RAP1B protein expression. This study revealed the chemical components of FPB-TA and explored its potential molecular mechanism for alleviating PF, providing a theoretical basis and research direction for further in-depth exploration of its mechanism of action.