Key result
Network pharmacology and molecular experiments demonstrated that naringenin, an active compound in Citri Reticulatae Pericarpium, inhibits myocardial hypertrophy by regulating targets like AKT1 and MAPK3.
Why the study?
To screen the main active compounds of Citri Reticulatae Pericarpium, construct a drug-ingredient-disease-target network, explore its molecular mechanisms in treating myocardial hypertrophy, and validate findings using a molecular biology approach.
Network pharmacology and molecular experiments suggest naringenin from Citri Reticulatae Pericarpium may inhibit myocardial hypertrophy via multiple signaling pathways.
Hypothesis-generating for naringenin in hypertrophy; requires validation before any clinical consideration.
Objective: Through a network pharmacology method, we screened the main active compounds of Citri Reticulatae Pericarpium (CRP), constructed a drug-ingredient-disease-target network, explored the molecular mechanism of its treatment of myocardial hypertrophy, and validated it by using molecular biology approach. Methods: Traditional Chinese Medicine Systems Pharmacology (TCMSP) and GeneCards were utilised to collect the effective component in CRP and the targets of CRP and myocardial hypertrophy. The STRING database constructed the protein interaction network. The drug-ingredient-disease-target network was outlined by the Cytoscape 3.9.0 software. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted using the Metascape database. Real-time PCR (RT-PCR) and Western blotting were utilised to determine the mRNA and protein level of the critical targets of CRP therapy for myocardial hypertrophy. Results: We found that five practical components of CRP exerted therapeutic effects on myocardial hypertrophy by modulating 41 targets. Further analysis revealed that naringenin was the essential active compound in CRP that regulated myocardial hypertrophy. In addition, we showed that the active compounds of CRP might exert antihypertrophy effects via regulating essential target proteins such as AKT1-, MAPK3-, PPARA-, PPARG-, and ESR1-mediated signaling pathways such as cell proliferation, nuclear receptor activation, and oxidative stress. The molecular biology experiments demonstrated that naringenin inhibited the mRNA level of NPPA and NPPB induced by Ang II and regulated related targets such as AKT1, MAPK3, PPARA, PPARG, and ESR1. Conclusion: CRP could inhibit myocardial hypertrophy through multitarget and multiapproach.
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Jiang et al. (2022) studied Myocardial hypertrophy. Citri Reticulatae Pericarpium (CRP) / naringenin was evaluated on Molecular targets and pathways related to myocardial hypertrophy. Network pharmacology and molecular experiments demonstrated that naringenin, an active compound in Citri Reticulatae Pericarpium, inhibits myocardial hypertrophy by regulating targets like AKT1 and MAPK3.
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