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It was reported that GLP-1 (9-36) decreased the level of nuclear factor kappa-B (NF-B) in astrocytes after oxygen-glucose deprivation/reoxygenation (OGD/R) damage and inhibited neuronal apoptosis around the infarct area against CIR, the mechanism of which might be relying on the activation of the IGF-1 receptor rather than the GLP-1 receptor (91)

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This dual modulation of microbial ecology and host incretin physiology underscores leonurines unique therapeutic value

The peptide's ability to activate VEGFR2-nitric oxide signaling in bone tissue enhances bone matrix deposition and fracture consolidation