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TL;DR
The central result is that MBSYQ treatment alleviated bone loss and microstructure damage in model rats by activating MAPK and PI3K/AKT pathways.
Drug Design, Development and Therapy · 6 authors, 2 centres
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The central result is that MBSYQ treatment alleviated bone loss and microstructure damage in model rats by activating MAPK and PI3K/AKT pathways.
In silico analysis identified 228 therapeutic targets for MBSYQ, with KEGG enrichment highlighting MAPK and PI3K/AKT pathways. In the rat model, MBSYQ treatment alleviated lung pathology and reversed bone loss and microstructure damage in the femur and L1 vertebra. RNA sequencing showed MBSYQ upregulated genes linked to anti-oxidative stress and aerobic respiration, and GSEA analysis confirmed it activated the MAPK and PI3K/AKT pathways inhibited by CS exposure. The study suggests MBSYQ may improve oxygen metabolism and activate these pathways to treat the condition. Limitations include the use of young rats and whole-body CS exposure, which may not fully reflect human disease.