ArticleMedicine2025
Study on mechanism of iridoid glycosides derivatives from Fructus Gardeniae in treatment of hepatic encephalopathy by network pharmacology and molecular docking technology.
Article in Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundThis study aims to explore the mechanism of the iridoid glycosides from Fructus Gardeniae (IGFG) in treating hepatic encephalopathy (HE) by combining network pharmacology and molecular docking technology.
methodsFirstly, we collected the targets of IGFG and HE. The targets of IGFG were predicted through the CTD, SWISS and TCMSP database and the targets of HE were screened through the DisGeNET database. Then the targets of IGFG and HE were mapped to attain the common target of IGFG in treating HE. Then, chemicals-target-disease network was constructed. Secondly, we constructed protein-protein interactions (PPI) network using STRING database and Cytoscape software. Moreover, we screened the core targets according to the degree value. Thirdly, the mechanism of IGFG in treating HE was revealed by Gene ontology and KEGG enrichment analysis. Meanwhile, chemicals-target-pathway network was constructed. Finally, to further verify the analysis results, molecular docking study was conducted.
resultsNetwork pharmacology indicates that there are 12 common targets between IGFG and HE. Eleven core targets were identified by the construction of PPI network. Association for core targets, and related pathways was analyzed, implying that core targets related to these pathways are AKT1, tumor necrosis factor, MTOR, CHUK, PPP2CA, IKBKB, AKT2, IKBKG, IL1B, NFKBIA, and CASP8. The main mechanism of IGFG in treating HE is closely related to inhibit inflammatory reaction, regulate immunity, promote hepatocyte regeneration, reduce hepatocyte apoptosis, maintain liver function homeostasis and antiviral function. Finally, the results of molecular docking showed that the binding free energy of geniposide with the core target was less than -5 kJ/mol, which indicated that geniposide could spontaneously bind to the receptor protein and had strong binding force.
conclusionIGFG can achieve simultaneous intervention of HE by inhibit inflammatory reaction, regulate immunity, promote hepatocyte regeneration, reduce hepatocyte apoptosis, maintain liver function homeostasis and antiviral function. It presents the network regulation mechanism of mutual influence and complex correlation. This study provides a scientific basis for IGFG in the treatment of patients with HE.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.