Background and objectives: Obstructive sleep apnoea (OSA) can result in chronic intermittent hypoxia (CIH), which triggers an inflammatory response. Banxia-Houpu Decoction (BHD) has been reported to ameliorate cardiac injury induced by OSA. The aim of this study was to elucidate the molecular basis and therapeutic role of BHD in CIH-induced myocardial injury.
Aim: The aim of this study was to investigate the therapeutic potential of BHD in the treatment of OSA by examining its bioactive components, target genes, molecular interactions, pathways, and therapeutic efficacy.
Materials and methods: C57BL/6 N mice were randomly divided into control, CIH, BHD-L (7.02 g/kg/d) and BHD-H (14.04 g/kg/d) groups. The mice were exposed to CIH (21-5 % O2, 20 times/h, 8 h/d) for 28 d. An aqueous extract of BHD was analysed using LC-MS/MS. Cardiac function, network pharmacology, inflammation levels, apoptosis, and molecular docking were analysed.
Results: BHD significantly reduced cardiac function impairment and cardiac enzyme levels caused by CIH. Hypoxia-inducible factor 1-α (HIF1-α) was identified as a therapeutic target through network pharmacology and gene transcriptomics. BHD downregulated HIF1-α expression and inhibited the transition of macrophages from the M2 phenotype to the M1 phenotype by increasing CD163 expression while downregulating inducible nitric oxide synthase (iNOS) and CD68 levels. BHD decreased pro-inflammatory factor levels and increased anti-inflammatory factor levels. Finally, the results of molecular docking and kinetic simulations demonstrated that the active components of BHD effectively bind to HIF1-α.
Conclusion: These findings highlight that BHD attenuates CIH-induced cardiomyocyte-mediated inhibition of the HIF1-α-inflammatory pathway.
Keywords: Cardiovascular disease; Chronic intermittent hypoxia; Hypoxia-inducible factor-1α; Inflammation; Obstructive sleep apnea.
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