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Baicalin maintained redox balance and inhibited PI3K/AKT pathway via binding with AKT to ameliorated LPS induced cardiac injury

ABSTRACT: Purpose The aim of this study was to investigate the effects of baicalin on septic cardiomyopathy and to elucidate the underlying mechanisms involved. Specifically, this study sought to determine the effects of baicalin on septic cardiomyopathy induced by AC16 cells and LPS in C57BL/6J mice and its underlying mechanisms. Methods: Echocardiography, histological staining, immunoblotting, qPCR, ELISA, RNA-seq, network pharmacology and molecular docking were performed. Changes in cardiomyocytes after LPS injection in mice were observed. The targets of baicalein in septic cardiomyopathy were screened using molecular docking and molecular dynamics, and the pathway of baicalein action was further elucidated by using RNA-seq and network pharmacology. Results: LPS stimulation induced apoptosis, an inflammatory response and oxidative stress in cardiomyocytes. In vivo experiments revealed that baicalin treatment attenuated septic myocardial injury, as evidenced by enhanced cardiac functional parameters, preservation of myocardial structure, and reduced inflammatory/apoptotic responses, and RNA-seq analyses revealed that the Pi3k/AKT signaling pathway was activated after the administration of baicalin, which was verified both in vitro and in vivo; this indicated that the protective effects of baicalin were related to the findings in vitro and in vivo, suggesting that the protective effect of baicalin is related to the activation of the PI3K/AKT pathway. Molecular docking studies revealed that baicalin inhibited cardiomyocyte inflammation and cardiomyocyte apoptosis, thereby ameliorating sepsis-induced cardiac injury, which may be related to the PI3K/Akt pathway. Conclusion: Baicalin activates the PI3K/AKT pathway and protects against sepsis-induced cardiac injury by binding with AKT.

ORGANISM(S): Mus musculus

PROVIDER: GSE292359 | GEO | 2026/03/24

REPOSITORIES: GEO

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Project description:Osteoarthritis (OA) is a debilitating joint disorder characterized by cartilage degradation and chondrocyte homeostasis disruption. Although retinoic acid (RA) has been applied in the model preparation of OA, its target of action and signaling pathway are not clear. Leveraging a translational framework that integrates RNA-sequencing transcriptomics, network pharmacology prediction, computational ligand-receptor molecular docking, and biological experimental validation, this study systematically deciphers RA's disease-modifying targets and associated signaling circuitry in OA pathogenesis. RNA-sequencing of RA-treated chondrocytes revealed 656 differentially expressed genes (DEGs). Protein-protein interaction (PPI) network analysis and functional enrichment (GO/KEGG) highlighted key pathways, including extracellular matrix reorganization and PI3K-Akt-mediated mechanotransduction and others. Additionally, molecular docking results ranked binding affinities in descending order as follows: ACAN > SFRP2 > KANSL2 (NSL2), and so on. Network pharmacology identified 42 RA-OA shared targets, with protein-protein interaction (PPI) analysis and functionally enriched (GO/KEGG) including the Renin-angiotensin system, Neuroactive ligand-receptor interaction, and others. The molecular docking results showed a total score in descending order of MAPK14(p38α), PTGER3(PGE2-R), CA2(CACNA2D2), and so on. Five intersecting targets (CA2, ACE, PTGS1(COX-1), PGR, and EDNRA(ETAR) ) from RNA-sequencing and network pharmacology were obtained, and molecular docking was used to dock the intersecting targets to RA. The docking results demonstrated strong binding affinities, which were further validated through western blot and RT-qPCR experiments, confirming the RA-induced upregulation of the intersecting targets. These findings were accompanied by immunofluorescent evidence showing elevated levels of MMP13 and suppressed expression of COL2A1, collectively reflecting the phenotypic characteristics of OA. Our findings position CA2 and ACE as key hubs for multi-targeting. This study not only reveals possible mechanistic studies of RA in OA but also provides a drug reference for the development of drugs against OA.

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Baicalin maintained redox balance and inhibited PI3K/AKT pathway via binding with AKT to ameliorated LPS induced cardiac injury

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