Mogroside V: Molecular mechanisms and therapeutic applications

Mogroside V (MV) constitutes the primary bioactive compound within Siraitia grosvenorii and has significant therapeutic effects on oxidative stress, inflammation, osteoporosis, diabetes, obesity, and nervous system damage. Presently, there exists a shortage of comprehensive reviews explaining its therapeutic mechanisms through core signaling pathways.

To systematically organize and summarize recent advances MV's molecular mechanisms and its therapeutic potential.

The potential mechanisms of MV on the above diseases were explored by searching relevant literature published in databases such as PubMed, Web of Science, and Google Scholar, combined with the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis.

MV mediates its multifaceted biological functions via key signaling cascades. Anti-inflammatory actions are facilitated through pathways of Janus kinase/signal transducer and activator of transcription (JAK/STAT), Protein kinase B/ phosphatidylinositol 3-kinase/mechanistic target of rapamycin (PI3K/Akt/mTOR), Toll-like receptor 4 (TLR4), and Endoplasmic reticulum stress (ERS)-unfolded protein response (ERS-UPR). For anti-oxidant defense, MV predominantly engages the Nuclear (factor erythroid 2-related factor 2/heme oxygenase 1) Nrf2/HO-1, PI3K/Akt, and sirtuin (SIRT) pathways. Furthermore, MV regulates metabolism and offers therapeutic potential by targeting the AMP-activated Protein Kinase (AMPK) pathway in obesity, modulating the PI3K/Akt/ glucose transporter type 2(GLUT2) axis for diabetes management, and activating the Taurine Upregulated Gene 1 (TUG1) pathway to enhance osteogenesis.

MV is a promising multi-target therapeutic candidate. Further studies on bioavailability optimization and clinical translation are warranted.