Nature Scientific Reports independent verification
Hsieh et al./Nature/2020
Why It Matters
This paper caught my attention because it's one of the first to map out exactly how BPC 157 might affect blood vessels — something relevant given the peptide's popularity in recovery circles. The nitric oxide pathway they identified is the same one that exercise and certain supplements target for cardiovascular benefits. But let's be clear: this is isolated rat tissue in a lab, not humans taking BPC 157 orally or by injection. The mechanism is interesting, but we're several steps away from knowing if this translates to actual cardiovascular benefits in people.
Key Findings
- BPC 157 caused dose-dependent vasodilation (blood vessel relaxation) in isolated rat aortic tissue, with the effect almost entirely dependent on intact endothelium (the inner lining of blood vessels)
- The vasodilation effect was mediated by nitric oxide production — blocking NO synthesis with L-NAME eliminated most of the effect
- BPC 157 activated a specific molecular pathway: it triggered Src kinase phosphorylation, which led to Caveolin-1 phosphorylation, which released eNOS (endothelial nitric oxide synthase) to produce NO — blocking Src eliminated this cascade
- BPC 157 reduced the binding between Caveolin-1 and eNOS, effectively freeing eNOS to become active and produce nitric oxide
- BPC 157 promoted migration of vascular endothelial cells in culture, potentially relevant to its reported tissue repair effects