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The mechanism likely involves the same angiogenic pathway: bone repair is acutely dependent on vascularization of the fracture gap, and BPC-157's VEGF-stimulating activity addresses this bottleneck directly

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In both groups, lixisenatide markedly ameliorated neurological deficit, reduced infarct volume, along with inhibited the expression of oxidative stress parameters (GSH, MDA, NO and catalase enzyme), apoptotic marker (caspase-3), and inflammatory factor (TNF-) in ischemic brains of rats (117)

Eur Heart J 27(19):23382345 Levitan EB, Wolk A, Mittleman MA (2009) Relation of consistency with the dietary approaches to stop hypertension diet and incidence of heart failure in men aged 45 to 79 years