ArticleDrug design, development and therapy2025
6-Hydroxygenistein Ameliorates High Altitude Brain Injury via Activating PI3K/AKT Signaling Pathway Based on Transcriptomic Analysis and Experimental Validation.
Article in Drug design, development and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: Our Prior research has shown that 6-hydroxygenistein (6-OHG) alleviates hypobaric hypoxia induced brain injury (HHBI) achieved by its powerful antioxidant, anti-inflammatory, and anti-apoptotic capabilities, but its mechanism still requires additional investigation. The objective of this study was to uncover the protective mechanism of 6-OHG against HHBI based on transcriptomics analysis and experimental validation. Methods: The gene levels in brain tissue obtained from previous study were accessed via the RNA-Seq technique. DESeq2 R package was used to identify the differentially expressed genes (DEGs). Functional enrichment analysis and molecular docking were investigated utilizing the clusterProfiler R package and Autodock Vina software, respectively. In experimental validation stage, histological analysis was performed using Hematoxylin-Eosin (HE) staining. Oxidative stress, inflammatory, and apoptotic indexes in brain tissue were measured using commercial kits. Western blot was applied for detecting related protein expression. Results: The RNA-Seq analysis revealed 905 differentially expressed genes (DEGs) between the Con and Mod groups, with 239 upregulated and 666 downregulated. Between the 6-OHG and Mod groups, there were 192 DEGs, including 98 upregulated and 94 downregulated genes. Go and KEGG function analyses highlighted the PI3K/AKT signaling pathway as a crucial regulatory mechanism. Western blot analysis showed that HH exposure caused a decrease in the ratios of p-PI3K/PI3K and p-AKT/AKT in the mouse brain, but this effect was reversed by 6-OHG treatment, indicating that 6-OHG activates the PI3K/AKT signaling pathway. Furthermore, LY294002, a selective PI3K inhibitor, effectively blocked this activation and also abolished the protective effects of 6-OHG on histopathological damage, as well as its antioxidant, anti-inflammatory, and anti-apoptotic activities in HHBI mice. Conclusion: 6-OHG mitigates HHBI by activating the PI3K/AKT signaling pathway, suggesting its potential therapeutic application for HHBI treatment.
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