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The 500 mcg per-capsule dose mirrors the per-day intake used in the bulk of rodent oral studies, and the gastric origin of the parent molecule provides a biological rationale for stability through the GI tract a feature documented across multiple oral-administration preclinical models
The GSSG thus generated is converted back to GSH, either by de novo synthesis or enzymatically by GR
This activation leads to the stimulation of the VEGFR2-Akt-eNOS signaling pathway, enhancing endothelial tube formation and blood flow recovery in ischemic tissues
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